Showing papers on "Sodium arsenite published in 2016"

Antioxidant Potential of Spirulina platensis Mitigates Oxidative Stress and Reprotoxicity Induced by Sodium Arsenite in Male Rats

Abstract: The present study aimed to examine the protective role of Spirulina platensis (S. platensis) against arsenic-induced testicular oxidative damage in rats. Arsenic (in the form of NaAsO2 at a dose of 6.3 mg/kg body weight for 8 weeks) caused a significant accumulation of arsenic in testicular tissues as well as a decrease in the levels of testicular superoxide dismutase (SOD), catalase (CAT), reduced glutathione, and zinc. Moreover, it significantly decreased plasma testosterone, luteinizing hormone (LH), triiodothyronine (T3), and thyroxine (T4) levels and reduced sperm motility and sperm count. Arsenic (AS) led to a significant increase in testicular malondialdehyde (MDA), tumour necrosis factor alpha (TNF-α), nitric oxide (NO), and sperm abnormalities. S. platensis at a dose of 300 mg/kg was found to attenuate As-induced oxidative stress, testicular damage, and sperm abnormalities by its potent antioxidant activity. S. platensis may represent a potential therapeutic option to protect the testicular tissue from arsenic intoxication.

Effects of sodium arsenate and arsenite on male reproductive functions in Wistar rats.

Abstract: Arsenic (As), in the form of trivalent arsenite or pentavalent arsenate, is a ubiquitous toxic compound naturally occurring in the environment. This study aimed to evaluate the impact of two different forms of inorganic As on reproductive parameters following oral exposure. Adult Wistar male rats were exposed to sodium arsenite or arsenate at concentrations of 0.01 mg/L or 10 mg/L for 56 d in drinking water. Sodium arsenite at both concentrations and sodium arsenate at 10 mg/L produced reduction in daily sperm production, in number of spermatids in the testis, and in sperm in the epididymal caput/corpus regions. Changes in epididymal morphometry were variable and region specific. Total and progressive sperm motility and sperm morphology did not differ markedly between controls and animals exposed to As. The body and reproductive organs weights, as well as testosterone concentration, remained unchanged among all groups. In conclusion, As exposure in drinking water over 56 d produced damage in male reproductive functions in adult rats, suggesting that fertility problems might occur. Therefore, additional studies need to be undertaken to investigate potential mechanisms underlying sodium arsenite- and arsenate-induced disturbances in fertility and reproductive performance.

Protective effects of thymoquinone against apoptosis and oxidative stress by arsenic in rat kidney

Abstract: We aimed to investigate the protective role of thymoquinone (TQ) by targeting its antiapoptotic and antioxidant properties against kidney damage induced by arsenic in rats. We have used the 24 male Sprague-Dawley rats. Rats were divided into three groups. Physiological serum in 10 mL/kg dose as intragastric was given to the control group. Sodium arsenite (10 mg/kg, intragastric by gavage for fifteen days) was given to the arsenic group. Sodium arsenite (10 mg/kg, intragastric by gavage for fifteen days) and TQ (10 mg/kg, intragastric by gavage for 15 days) was given to the arsenic + TQ group. After 15 days, the animals' kidneys were taken theirs, then we have performed histological and apoptotic assessment. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzyme activities and malondialdehyde (MDA) levels have examined as the oxidative stress parameters. We have determined the levels of arsenic. Increased renal injury and apoptotic cells have been detected in the arsenic group. Degenerative changes in the arsenic + TQ group were diminished. Although the MDA levels were augmented in the arsenic group, SOD, CAT and GSH-Px enzyme activities were lessened than the other groups. Our findings suggest that TQ may impede the oxidative stress, the cells have been damaged and also the generation of apoptotic cells arisen from arsenic. TQ plays a protective role against arsenic-induced toxicity in kidney and may potentially be used as a remedial agent.

Protective effects of quercetin against arsenic-induced testicular damage in rats.

Abstract: Summary This study investigated the effect of quercetin on changes in testes due to arsenic exposure. Twenty-seven male rats were divided into three groups: control (10 ml kg−1 day−1 saline), arsenic (10 mg kg−1 day−1 sodium arsenite) and arsenic + quercetin (arsenic + 50 mg kg−1 day−1 quercetin). The rats were sacrificed at the end of 15-day experiment. There was no difference between control group and arsenic group in body weight gain, testicular weight and serum total testosterone level. Quercetin treatment did not cause a significant difference in these parameters. In the arsenic group rats, we determined deterioration in the structure of seminiferous tubules, a decrease in the number of spermatogenic cells, an increase in the number of apoptotic cells, a decrease in the number of PCNA-positive cells, a decrease in SOD, CAT and GSH-Px activities, and an increase in the MDA level in testicular tissue. In all these changes, arsenic+quercetin group showed an improved compared to arsenic group. The amount of arsenic increased in the arsenic group was compared to the control group, and there was no difference between arsenic group and arsenic + quercetin group in the amount of arsenic. In conclusion, quercetin prevented arsenic-induced testicular damage with its anti-apoptotic and antioxidant effects.

Attenuative role of mangiferin in oxidative stress-mediated liver dysfunction in arsenic-intoxicated murines.

Abstract: Mangiferin (MAG), a natural xanthone mainly derived from mangoes, possesses great antioxidative potentials. The present study has been carried out to investigate the hepato-protective role of MAG, against arsenic (As)-induced oxidative damages in the murine liver. As, a well-known toxic metalloid, is ubiquitously found in nature and has been reported to affect nearly all the organs of the human body via oxidative impairment. Administration of As in the form of sodium arsenite (NaAsO2 ) at a dose of 10 mg/kg body weight for 3 months abruptly increased reactive oxygen species (ROS) level, led to oxidative stress and significantly depleted the first line of antioxidant defense system in the body. Moreover, As caused apoptosis in hepatocytes. Treatment with MAG at a dose of 40 mg/kg for body weight for 30 days simultaneously and separately after NaAsO2 administration decreased the ROS production and attenuated the alterations in the activities of all antioxidant indices. MAG also protected liver against the NaAsO2 -induced apoptosis and disintegrated hepatocytes, thus counteracting with As-induced toxicity. It could significantly inhibit the expression of different proapoptotic caspases and upregulate the expression of survival molecules such as Akt and Nrf2. On inhibiting Akt (by PI3K inhibitor, LY294002) and ERK1/2 (by ERK1/2 inhibitor, PD98059) specifically, caspase 3 got activated abolishing mangiferin's protective role on As-induced hepatotoxicity. So here, we have briefly elucidated the signaling cascades involved in As-induced apoptotic cell death in the liver and also the detailed cellular mechanism by which MAG provides protection to this organ. © 2016 BioFactors, 42(5):515-532, 2016.

Oral nanoparticulate curcumin combating arsenic-induced oxidative damage in kidney and brain of rats

Abstract: Arsenic exposure through drinking water causes oxidative stress and tissue damage in the kidney and brain. Curcumin (CUR) is a good antioxidant with limited clinical application because of its hydrophobic nature and limited bioavailability, which can be overcome by the encapsulation of CUR with nanoparticles (NPs). The present study investigates the therapeutic efficacy of free CUR and NP-encapsulated CUR (CUR-NP) against sodium arsenite-induced renal and neuronal oxidative damage in rat. The CUR-NP prepared by emulsion technique and particle size ranged between 120 and 140 nm, with the mean particle size being 130.8 nm. Rats were divided into five groups (groups 1-5) with six animals in each group. Group 1 served as control. Group 2 rats were exposed to sodium arsenite (25 ppm) daily through drinking water for 42 days. Groups 3, 4, and 5 were treated with arsenic as in Group 2; however, these animals were also administered with empty NPs, CUR (100 mg/kg body weight), and CUR-NP (100 mg/kg), respectively, by oral gavage during the last 14 days of arsenic exposure. Arsenic exposure significantly increased serum urea nitrogen and creatinine levels. Arsenic increased lipid peroxidation (LPO), reduced glutathione content and the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase were depleted significantly in both kidney and brain. Treatment with free CUR and CUR-NP decreased the LPO and increased the enzymatic and nonenzymatic antioxidant system in kidney and brain. Histopathological examination showed that kidney and brain injury mediated by arsenic was ameliorated by treatment. However, the amelioration percentage indicates that CUR-NP had marked therapeutic effect on arsenic-induced oxidative damage in kidney and brain tissues.

Effects of Sodium Arsenite and Arsenate in Testicular Histomorphometry and Antioxidants Enzymes Activities in Rats

Abstract: The main source of environmental arsenic exposure in most countries of the world is drinking water in which inorganic forms of arsenic predominate. The present study was aimed to test the impact of two different compounds of inorganic arsenic in histomorphometric and enzymatic parameters in the testes by oral exposition. Adult Wistar male rats were exposed to sodium arsenite and arsenate in drinking water, testing for each chemical form the concentrations of 0.01 and 10 mg/L per 56 days. The animals intoxicated with arsenic, mainly sodium arsenite, showed reduction in the percentage of seminiferous epithelium and in proportion and volume of Leydig cells. Moreover, there was an increase in the percentage of tunica propria, lumen, lymphatic space, blood vessels, and macrophages. The activity of superoxide dismutase (SOD) did not change among the groups. However, the activity of catalase (CAT) decreased in animals exposed to both arsenic compounds. In addition, the higher concentration of arsenic, mainly as sodium arsenite, caused vacuolization in the seminiferous epithelium. The body and testes weight as well as testosterone concentration remained unchanged among the groups. In conclusion, exposition to arsenic, mainly as sodium arsenite, caused alteration in histomorphometric parameters and antioxidant defense system in the testes.

Effect of Acetyl-L-Carnitine on Antioxidant Status, Lipid Peroxidation, and Oxidative Damage of Arsenic in Rat.

Abstract: Arsenic (As) is a widespread environmental contaminant present around the world in both organic and inorganic forms. Oxidative stress is postulated as the main mechanism for As-induced toxicity. This study was planned to examine the protective effect of acetyl-L-carnitine (ALC) on As-induced oxidative damage in male rats. Animals were randomly divided into four groups of control (saline), sodium arsenite (NaAsO2, 20 mg/kg), ALC (300 mg/kg), and NaAsO2 plus ALC. Animals were dosed orally for 28 successive days. Blood and tissue samples including kidney, brain, liver, heart, and lung were collected on the 28th day and evaluated for oxidative damage and histological changes. NaAsO2 exposure caused a significant lipid peroxidation as evidenced by elevation in thiobarbituric acid-reactive substances (TBARS). The activity of antioxidant enzymes such as glutathione-S-transferase (GST), catalase (CAT), superoxide dismutase (SOD), as well as sulfhydryl group content (SH group) was significantly suppressed in various organs following NaAsO2 treatment (P < 0.05). Furthermore, NaAsO2 administration increased serum values of alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and bilirubin. Our findings revealed that co-administration of ALC and NaAsO2 significantly suppressed the oxidative damage induced by NaAsO2. Tissue histological studies have confirmed the biochemical findings and provided evidence for the beneficial role of ALC. The results concluded that ALC attenuated NaAsO2-induced toxicity, and this protective effect may result from the ability of ALC in maintaining oxidant-antioxidant balance.

Arsenic induced hematological and biochemical responses in nutritionally important catfish Clarias batrachus (L.)

Abstract: The impact of sublethal toxicity of sodium arsenite on hematological and certain biochemical parameters of the fresh water catfish Clarias batrachus has been analyzed following exposure of sublethal concentration (1 mg/L; 5% of LC50 value) of sodium arsenite for 10, 30, 45, and 60 days. Arsenic bioaccumulation in the blood tissue of the fish increased progressively with increased period of exposure. The values of total erythrocyte count (TECs), total leucocytes count (TLCs), hemoglobin concentration, and packed cell volume (PCV) 1.40 ± 0.03 × 106/mm3, 174.83 ± 2.74 × 103/mm3, 5.01 ± 0.26 g/100 ml, 25.00 ± 1.06 were observed respectively at the end of 60 days of exposure. The results of hematological indices were found to be 179.23 ± 8.81fl/cell for mean corpuscular volume (MCV), 35.92 ± 1.89 pg/cell for mean corpuscular hemoglobin (MCH) and 20.17 ± 1.12 g/dl for mean corpuscular hemoglobin concentration (MCHC). The present findings are clearly indicating severe fish anemia due to the arsenic salt exposure. The continued arsenic toxicity results in decreased serum protein concentration that might be a cause for the loss of weight as well as weakness in the fish.

Oxidative DNA damage enhances the carcinogenic potential of in vitro chronic arsenic exposures.

Abstract: Chronic exposure to arsenic is known to increase the incidence of cancer in humans. Our previous work demonstrated that environmentally relevant arsenic exposures generate an accelerated accumulation of pre-carcinogen 8-OH-dG DNA lesions under Ogg1-deficient backgrounds, but it remains unproved whether this observed arsenic-induced oxidative DNA damage (ODD) is certainly important in terms of cancer. Here, isogenic MEF Ogg1 +/+ cells and MEF Ogg1 −/− cells—unable to properly eliminate 8-OH-dG from DNA—were exposed to 0.5, 1 and 2 µM of sodium arsenite for 40 weeks. The acquisition of an in vitro cancer-like phenotype was assessed throughout the exposure; matrix metalloproteinase (MMP) activities were measured by zymography, colony formation and promotion were evaluated by soft agar assay, and cellular invasiveness was measured by the transwell assay. Alterations in cellular morphology, growth and differentiation status were also included as complementary measures of transformation. MEF Ogg1 −/− cells showed a cancer-associated phenotype after 30 weeks of exposure, as indicated by morphological changes, increased proliferation, deregulated differentiation status, increased MMPs secretion, anchorage-independent cell growth and enhancement of tumor growth and invasiveness. Conversely, MEF Ogg1 +/+ cells did not present changes in morphology or proliferation, exhibited a milder degree of gene deregulation and needed 10 weeks of additional exposure to the highest arsenite doses to show tumor enhancing effects. Thus, Ogg1 genetic background and arsenic-induced 8-OH-dG proved relevant for arsenic-mediated carcinogenic effects. To our knowledge, this is the first study directly linking ODD with arsenic carcinogenesis.

Oxidative stress-related liver dysfunction by sodium arsenite: Alleviation by Pistacia lentiscus oil

Abstract: Context: Pistacia lentiscus L. (Anacardiaceae) is an evergreen shrub widely distributed throughout the Mediterranean region. Pistacia lentiscus oil (PLo) was particularly known in North African traditional medicine. Thus, people of these regions have used it externally to treat sore throats, burns and wounds, as well as they employed it internally for respiratory allergies. PLo is rich in essential fatty acids, vitamin E and polyphenols. As a very active site of metabolism, liver is reported to be susceptible to arsenic (As) intoxication.Objective: The present study evaluates the protective effect of PLo against sodium arsenite-induced hepatic dysfunction and oxidative stress in experimental Wistar rats.Materials and methods: Twenty-eight rats were equally divided into four groups; the first served as a control, the remaining groups were respectively treated with PLo (3.3 mL/kg body weight), sodium arsenite (5.55 mg/kg body weight) and a combination of sodium arsenite and PLo. After 21 consecutive...

Protective effect of silymarin on viability, motility and mitochondrial membrane potential of ram sperm treated with sodium arsenite.

Abstract: Background: Sodium arsenite can impair male reproductive function by inducing oxidative stress. Silymarin is known as a potent antioxidant.Objective: This study was performed to investigate if silymarin can prevent the adverse effect of sodium arsenite on ram sperm viability, motility and mitochondrial membrane potential.Materials and Methods: Epidydimal spermatozoa obtained from ram were divided into five groups: 1) Spermatozoa at 0 hr, 2) spermatozoa at 180 min (control), 3) spermatozoa treated with sodium arsenite (10 μM) for 180 min, 4) spermatozoa treated with silymarin (20 μM) + sodium arsenite (10 μM) for 180 min and 5) spermatozoa treated with silymarin (20 μM) for 180 min. MTT assay and Rhodamine 123 staining were used to assess sperm viability and mitochondrial membrane potential respectively. Sperm motility was performed according to World Health Organization (WHO) guidelines.Results: Viability (p<0.01), nonprogressive motility (p<0.001) and intact mitochondrial membrane potential (p<0.001) of the spermatozoa were significantly decreased in sodium arsenite treated group compared to control group. In silymarin + sodium arsenite group, silymarin could significantly reverse the adverse effect of sodium arsenite on these sperm parameters compared to sodium arsenite group (p<0.001). In addition, the application of silymarin alone for 180 minutes could significantly increase progressively motile sperm (p<0.001) and decrease non motile sperm (p<0.01) compared to the control.Conclusion: Silymarin could compensate the adverse effect of sodium arsenite on viability, nonprogressive motility and mitochondrial membrane potential of ram sperm.

Arsenic and smokeless tobacco induce genotoxicity, sperm abnormality as well as oxidative stress in mice in vivo

Abstract: Arsenic, a naturally occurring metalloid is a well-known water contaminant which causes a wide range of serious adverse health effects including cancer upon long-term exposure. Recent studies have shown high arsenic contamination in the ground water of North Eastern states of India including Southern Assam. Smokeless tobacco consumption locally known as “sadagura” is one of the most prevalent life style habit in southern Assam. The present study was undertaken in mice test system in vivo. Mice were exposed to smokeless tobacco (5 mg/kg body weight /day) and sodium arsenite (0.2 mg/kg body weight /day, 2 mg/kg body weight/day) independently and in combination for 90 days. The results were compared with groups with only sodium arsenite exposure and groups which were exposed to only smokeless tobacco extract. Genotoxicity was evaluated by studying the incidence of micronucleated polychromatic erythrocytes from bone marrow. Both the tested doses of sodium arsenite induced statistically significant micronucleated polychromatic erythrocytes as compared to control group, however, sodium arsenite and smokeless tobacco extract could not increase the incidence of micronucleated polychromatic erythrocytes as compared to their individual counterparts when treated in combination in mice test system. Germ cell toxicity was evaluated by recording the sperm head abnormalities and total sperm count. Combined treatment of sodium arsenite and smokeless tobacco extract in lower dose induced a significant increase in sperm head abnormality as compared to only sodium arsenite and smokeless tobacco extract. Liver, kidney and intestine tissues were analyzed for various oxidative stress evaluations such as lipid peroxidation (MDA), Glutathione (GSH) and superoxide dismutase (SOD) assay. Sodium arsenite in combination with smokeless tobacco extract show higher genotoxic and germ cell toxic effects as compared to control but not when compared to their individual counterparts. Impairment of the sperm head morphology by sodium arsenite and smokeless tobacco extract alone and in combination with lower dose of sodium arsenite could be oxidative stress mediated effects. Besides, combination treatment of both the agents may not produce additive effects related to micronucleated polychromatic erythrocytes induction and decline of total sperm count.

Identification of Methylated Dithioarsenicals in the Urine of Rats Fed with Sodium Arsenite

Abstract: Biotransformation of inorganic arsenic results in the formation of methylarsenicals of both oxygen and sulfur analogues. Aiming to improve our understanding of metabolism of inorganic arsenic in animals, we conducted an animal feeding study with an emphasis on identifying new arsenic metabolites. Female F344 rats were given 0, 1, 10, 25, 50, and 100 μg/g of arsenite (iAsIII) in the diet. Arsenic species in rat urine were determined using high performance liquid chromatography (HPLC) separation and inductive coupled plasma mass spectrometry (ICPMS) and electrospray ionization tandem mass spectrometry (ESI MS/MS) detection. Nine arsenic species were detected in the urine of the iAsIII-dosed rats. Seven of these arsenic species were consistent with previous reports, including iAsIII, arsenate, monomethyarsonic acid, dimethylarsinic acid, trimethylarsine oxide, monomethylmonothioarsonic acid, and dimethylmonothioarsinic acid. Two new methyldithioarsencals, monomethyldithioarsonic acid (MMDTAV) and dimethyldit...

Sodium arsenite inhibited genomic estrogen signaling but induced pERα (Ser118) via MAPK pathway in breast cancer cells

Abstract: Arsenic (As) is considered a major environmental health threat worldwide due to its widespread contamination in drinking water. Recent studies reported that arsenic is a potential xenoestrogen as it interfered with the action of estrogen (E2) and estrogen receptor (ER) signaling. The present study investigated the effects of sodium arsenite (NaAsO2 ) on estrogen signaling in human breast cancer cells. The results demonstrated that NaAsO2 dose-dependently increased viability of hormone-dependent breast cancer MCF-7 and T47D cells expressing both ERα and ERβ but not hormone-independent MDA-MB-231 cells expressing ERβ. These suggested ERα contribution to NaAsO2 -stimulated breast cancer cells growth. NaAsO2 induced down-regulation of ERα but up-regulation of ERβ protein expressions in T47D cells. Moreover, NaAsO2 dose-dependently inhibited E2-induced ER transcriptional activity as it decreased E2-mediated ERE-luciferase transcription activation and PgR mRNA transcription but increased pS2 mRNA transcription. However, NaAsO2 induced both rapid and sustained activation of ERK1/2 and increased in phosphorylation of ERα at serine 118 residue, c-fos and c-myc protein expressions. These results indicated that NaAsO2 interferes the genomic estrogen-signaling pathway but induces activation of a rapid nongenomic signal transduction through ERK1/2 pathway which may contribute to its proliferative effect on hormone-dependent breast cancer cells. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1133-1146, 2016.

Effect of sodium arsenite on reproductive organs of female Wistar rats.

Abstract: The present study was performed to investigate the subchronic effect of sodium arsenite on female Wistar rats. Mature female rats were divided into 4 groups of 12 animals each. Group I received distilled water, whereas the other 3 groups received sodium arsenite at 10, 30, and 50 µg/L doses for 60 days through drinking water. Half of the animals from each group were dissected after 30 days and the remaining after 60 days. A disruption in estrous cycle was observed with prolonged diestrous and metestrous phases. A significant increase in ovarian surface epithelium and follicular atresia was observed in treated rats (p ≤ .05). A significant decrease (p ≤ .05) in the uterine myometrium was observed. A significant increase (p ≤ .05) in the levels of lipid peroxidation along with decrease in the activities of antioxidant enzymes was observed. The results revealed that subchronic exposure of sodium arsenite causes degenerative changes in reproductive organs and induces oxidative stress in female rats.

N-acetylcysteine and meso-2,3-dimercaptosuccinic acid alleviate oxidative stress and hepatic dysfunction induced by sodium arsenite in male rats.

Abstract: Environmental exposure to arsenic represents a serious challenge to humans and other animals. The aim of the present study was to test the protective effect of antioxidant N-acetylcysteine (NAC) either individually or in combination with a chelating agent, meso-2,3-dimercaptosuccinic acid (DMSA), against sodium arsenite oral toxicity in male rats. Five groups were used: control; arsenic group (orally administrated in a concentration of 2 mg/kg body weight [b.w.]); the other three groups were orally administrated sodium arsenite in a concentration of 2 mg/kg b.w. followed by either NAC (10 mg/kg b.w., intraperitoneally [i.p.]), DMSA (50 mg/kg b.w., i.p.) or NAC plus DMSA. Arsenic toxicity caused significant rise in serum aspartate aminotransferase, alanine aminotransferase and total bilirubin, and a significant decrease in total protein (TP) and albumin levels after 3 weeks of experimental period. In addition, arsenic-treated rats showed significantly higher arsenic content in liver and significant rise in hepatic malondialdehyde level. By contrast, sharp decreases in glutathione content and catalase and glutathione reductase activities were discernible. NAC and/or DMSA counteracted most of these physiologic and biochemical defects. NAC monotherapy was more effective than DMSA in increasing TP, while DMSA was more effective in decreasing alanine aminotransferase. The combined treatment was superior over monotherapies in recovery of TP and glutathione. Biochemical data were well supported by histopathological and ultrastructural findings. In conclusion, the combination therapy of NAC and DMSA may be an ideal choice against oxidative insult induced by arsenic poisoning.

Acute Sodium Arsenite-Induced Hematological and Biochemical Changes in Wistar Rats: Protective Effects of Ethanol Extract of Ageratum conyzoides

Abstract: Background: Ageratum conyzoides L. (Asteraceae) is an annual herbaceous plant used in folklore medicine for the treatment of a wide range of diseases. Objective: To investigate the protective effect of the ethanol leaf extract of A. conyzoides (EEAC) against hematological, serum biochemical and histological alterations induced by Sodium arsenite administration to Wistar rats. Materials and Methods: Twenty male Wistar rats were randomly assigned into four groups of five rats each. Group I received propylene glycol and Group II rats were given the (EEAC, 100 mg/kg b.w.) orally for 7 days. Group III were given a single oral dose of sodium arsenite (NaAsO2, 2.5 mg/kg b.w.). Animals in Group IV were pretreated with 100 mg/kg EEAC for 7 days followed by a single oral dose of sodium arsenite. Results: Arsenic exposure resulted in significant reductions (P < 0.05) in values of packed cell volume (PCV), hemoglobin concentration (Hb) and red blood cell (RBC) count, and elevation in total white blood cell (WBC) count with insignificant reductions in serum total protein, albumin, and globulin levels. Alterations in aspartate aminotransferase, alanine transferase, alkaline phosphatase, and gamma glutamyl transferase activities, as well as in serum levels of urea, creatinine, glucose, cholesterol, and triglyceride levels, were not statistically significant. EEAC significantly restored (P < 0.05) the PCV, Hb, RBC, and WBC as well as serum albumin, globulin, and total protein to normal values. Conclusion: The results of this study indicate that EEAC possess strong potentials to protect against toxicities induced by sodium arsenite.

Silymarin protects plasma membrane and acrosome integrity in sperm treated with sodium arsenite.

Abstract: Background: Exposure to arsenic is associated with impairment of male reproductive function by inducing oxidative stress. Silymarin with an antioxidant property scavenges free radicals. Objective: The aim of this study was to investigate if silymarin can prevent the adverse effects of sodium arsenite on ram sperm plasma membrane and acrosome integrity. Materials and Methods: Ram epidydimal spermatozoa were divided into five groups: spermatozoa at 0 hr, spermatozoa at 180 min (control), spermatozoa treated with silymarin (20 μM) + sodium arsenite (10 μM) for 180 min, spermatozoa treated with sodium arsenite (10 μM) for 180 min and spermatozoa treated with silymarin (20 μM) for 180 min. Double staining of Hoechst and propidium iodide was performed to evaluate sperm plasma membrane integrity, whereas comassie brilliant blue staining was used to assess acrosome integrity. Results: Plasma membrane (p< 0.001) and acrosome integrity (p< 0.05) of the spermatozoa were significantly reduced in sodium arsenite group compared to the control. In silymarin + sodium arsenite group, silymarin was able to significantly (p< 0.001) ameliorate the adverse effects of sodium arsenite on these sperm parameters compared to sodium arsenite group. The incubation of sperm for 180 min (control group) showed a significant (p< 0.001) decrease in acrosome integrity compared to the spermatozoa at 0 hour. The application of silymarin alone for 180 min could also significantly (p< 0.05) increase sperm acrosome integrity compared to the control. Conclusion: Silymarin as a potent antioxidant could compensate the adverse effects of sodium arsenite on the ram sperm plasma membrane and acrosome integrity.

Arsenite accumulation in the mouse eye.

Abstract: Elevated arsenic (As) concentrations in drinking water are a major worldwide public health concern. Exposure to As is associated with carcinogenesis, skin lesions, cardiovascular disease, cognitive deficits, and other disorders. However, little is known regarding chronic As-mediated effects on the eye. Oxidative stress is believed to be an important factor in As-related pathology and is also implicated in certain eye diseases such as cataract. Thus, elevated exposure to arsenic could potentially be a contributing factor for ocular pathology. A pilot study was therefore initiated to determine whether As could be detected in eye tissue of mice exposed to sodium arsenite in drinking water. Total As concentrations were determined by inductively coupled plasma-mass spectroscopy in whole eyes, lens, liver, heart, lung, kidneys, spleen, brain, and hair from mice given 0, 10, 50, or 250 ppm sodium arsenite in their drinking water for 4 wk or 0, 10 or 50 ppm for 6 mo. Dose-dependent increases in As concentration were observed in all organs and tissues. Surprisingly, As concentrations in the eye and lens were significantly higher than those in liver, lung, heart, spleen, and brain and similar to that found in kidneys. The relatively high concentration in the eye, and the lens in particular, suggests As exposure may be a contributing factor in cataract formation in parts of the world where As in drinking water is endemic.

Nanocurcumin Prevents Oxidative Stress Induced following Arsenic and Fluoride Co-exposure in Rats

Abstract: The present study is in continuation of our previous efforts to investigate the preventive efficacy of encapsulated curcumin nanoparticles (nanocurcumin) in mitigating effects of arsenic and/or fluoride. Curcumin was encapsulated in chitosan nanoparticles having a size distribution in the range of 50 nm. Sodium arsenite (2 mg/kg, orally) and Fluoride (50 ppm in drinking water) either alone or in combination were administered to male Wistar rats for four weeks to evaluate the efficacy of nanocurcumin (15 mg/kg) in rats. The preventive efficacy of nanocurcumin was evaluated against various altered biochemical variables suggestive of oxidative stress in liver and kidneys, and concentration of As and F in blood. Nanocurcumin co-administration with arsenic and fluoride resulted in lowering of reactive oxygen species and restoration of blood glutathione level which were found to be altered in arsenic and fluoride intoxicated groups. Nanocurcumin were also found to be effective in reversing δ-aminolevulinic acid dehydratase (ALAD) inhibition caused by arsenic exposure. The most promising result from our study shows that nanocurcumin removes not only arsenic but also fluoride from blood which may be due to the enhanced bioavailability and moderate chelating potential of nanocurcumin.

HEPATOPROTECTIVE EFFECT AND ANTIOXIDANT CAPACITY OF NARINGENIN ON ARSENIC- INDUCED LIVER INJURY IN RATS Original Article

Abstract: Objective: The present study was undertaken to evaluate the protective effect of naringenin (Ng) against arsenic (As)-induced oxidative stress in the liver of experimental rats. Arsenic is a major environmental pollutant and is known for its wide toxic manifestations. Naringenin is a naturally occurring citrus flavonone which has been reported to have a wide range of pharmacological properties. Methods: Forty male rats were randomly divided into four groups where the first was served as a control, whereas the remaining groups were respectively treated with naringenin (50 mg/kg b.w.), sodium arsenite (5.55 mg/kg b.w.) and a combination of sodium arsenite and naringen. Results: Exposure of rats to (As) caused a significant increase in liver MDA level compared to control, but the coadministration of (Ng) was effective in reducing its level. The enzymatic activities of glutathione peroxidase (GPx), and glutathione-S-transferase (GST), superoxide dismutase (SOD) and catalase(CAT)of As-treated group were found to be lower compared to the control and the (Ng)-treated group. On the other hand, a significant increase in activities of AST, ALT and ALP were observed in As-treated group. The co-administration of (Ng) has decreased the activities of AST, ALT and ALP and thus co-administration of (Ng) had an additive protective effect on liver enzyme activities and improved the antioxidant status as well. Conclusion: To conclude, the results suggest that As exposure enhanced an oxidative stress by disturbing the tissue antioxidant defense system, but the (Ng) co-administration protected liver tissues against As intoxication probably owing to its antioxidant properties.

Curcumin inhibits the adverse effects of sodium arsenite in mouse epididymal sperm

Abstract: The aim of this study was to investigate the effects of curcumin on epididymal sperm parameters in adult male Navel Medical Research Institute (NMRI) mice exposed to sodium arsenite..In this experimental study, we divided the animals into four groups: control, sodium arsenite (5 mg/kg), curcumin (100 mg/kg) and curcumin+sodium arsenite. Exposures were performed by intraperitoneal injections for a 5-week period. After the exposure period, we recorded the animals’ body and left testes weights. The left caudal epididymis was used to count the sperm number and analyze motility, viability, morphological abnormalities, acrosome reaction, DNA integrity, and histone-protamine replacement in the spermatozoa. One-way analysis of variance (ANOVA) followed by the Tukey’s test was used to assess the statistical significance of the data with SPSS 16.0. P<0.05 was considered significant..Mice exposed to sodium arsenite showed a significant decrease in the number, motility, viability, normal sperm morphology and acrosome integrity of spermatozoa compared to the control group. In the curcumin+sodium arsenite group, curcumin significantly reversed these adverse effects to the point where they approximated the control. In addition, the application of curcumin alone had no significant difference in these parameters compared to the control and curcumin+sodium arsenite groups. However, we observed no significant differences in the body and the testis weight as well as the DNA integrity and histone-protamine replacement in the spermatozoa of the four groups..Curcumin compensated for the toxic effects of sodium arsenite on a number of sperm parameters in adult mice.