Showing papers on "Sodium arsenite published in 2010"
TL;DR: Results indicate that arsenic disrupted the circulating levels of gonadotropins and estradiol, led to degeneration of luminal epithelial, stromal and myometrial cells of the rat uterus and downregulated the downstream components of the estrogen signaling pathway.
Abstract: Arsenic, a major pollutant of water as well as soil, is a known endocrine disruptor, and shows adverse effects on the female reproductive physiology. However, the exact molecular events leading to reproductive dysfunctions as a result of arsenic exposure are yet to be ascertained. This report evaluates the effect and mode of action of chronic oral arsenic exposure on the uterine physiology of mature female albino rats. The effect of chronic oral exposure to arsenic at the dose of 4 microg/ml for 28 days was evaluated on adult female albino rats. Hematoxylin-eosin double staining method evaluated the changes in the histological architecture of the uterus. Circulating levels of gonadotropins and estradiol were assayed by enzyme-linked immunosorbent assay. Expression of the estrogen receptor and estrogen-induced genes was studied at the mRNA level by RT-PCR and at the protein level by immunohistochemistry and western blot analysis. Sodium arsenite treatment decreased circulating levels of estradiol in a dose and time-dependent manner, along with decrease in the levels of both LH and FSH. Histological evaluation revealed degeneration of luminal epithelial cells and endometrial glands in response to arsenic treatment, along with reduction in thickness of the longitudinal muscle layer. Concomitantly, downregulation of estrogen receptor (ER alpha), the estrogen-responsive gene - vascular endothelial growth factor (VEGF), and G1 cell cycle proteins, cyclin D1 and CDK4, was also observed. Together, the results indicate that arsenic disrupted the circulating levels of gonadotropins and estradiol, led to degeneration of luminal epithelial, stromal and myometrial cells of the rat uterus and downregulated the downstream components of the estrogen signaling pathway. Since development and functional maintenance of the uterus is under the influence of estradiol, arsenic-induced structural degeneration may be attributed to the reduction in circulating estradiol levels. Downregulation of the estrogen receptor and estrogen-responsive genes in response to arsenic indicates a mechanism of suppression of female reproductive functions by an environmental toxicant that is contra-mechanistic to that of estrogen.
101 citations
TL;DR: The results concluded that the treatment with AECO prior to arsenic intoxication has significant role in protecting animals from arsenic-induced hepatic and renal toxicity.
97 citations
TL;DR: There is a dose-related accumulation of As species in all brain regions, with the highest accumulation observed in the pituitary, suggesting that AS3MT is ubiquitously expressed in the brain and it is not inducible by dose of arsenite.
88 citations
TL;DR: Pyrolusite (alpha-MnO(2) has important potential in arsenic transformation and removal as the environmentally friendly natural oxidant in soil and surface water and along with adsorption and fixation of arsenic species during the reaction.
80 citations
TL;DR: Co-administration of aqueous ginger extract with arsenite was found to protect against adverse change in the reproductive organ weight, attenuate the decrease in sperm functions, enhance plasma reproductive hormones level and increase antioxidants activities and reduced peroxidation.
Abstract: Arsenite is a major environmental chemical and a known reproductive toxicant via the depression of spermatogenesis and androgenesis in males. The possibility of sodium arsenite reproductive toxicity been caused by autooxidation was investigated in this study taking advantage of the anti-oxidant properties of ginger and its androgenic activities. The effect of exposure to sodium arsenite (10 mg/kg BW/day) by gavage via oral cannula without or with aqueous ginger extract (500mg/kg BW/day) co-treatments for 30 days was evaluated in adult male rats. The weight of the reproductive organs, sperm count, motility, and morphology were evaluated. Plasma FSH, LH and testosterone levels were assayed. Lipid peroxidation (indexed by MDA) and antioxidants enzymes likes GSH, SOD, CAT were assessed. Sodium arsenite treatment decreased the reproductive organs weight: testis, epididymis, prostate and seminal vesicle; sperm functions: count, motility and normal morphology; plasma hormones level: FSH, LH and testosterone. There was a decrease in the activities of GSH, SOD and CAT as well as an increase in MDA concentration. Co-administration of aqueous ginger extract with arsenite was found to protect against adverse change in the reproductive organ weight, attenuate the decrease in sperm functions, enhance plasma reproductive hormones level along with increased antioxidants activities and reduced peroxidation. This study showed that sodium arsenite apart from being a hormonal disrupter also causes oxidative stress which contributed to the reproductive damage in the male rats. The protective effects of ginger on reproductive toxicity and oxidative stress as evidenced by the clear restoration of sperm functions, testicular steroidogenesis and reproductive organo-somatic indices could be attributed to its antioxidants and androgenic properties. Key Words : Arsenite, Ginger, Antioxidants and Sperm.
79 citations
TL;DR: In this article, the arsenic detoxification potential of the bacterial strains was investigated with the arsenite oxidation gene, aox genotype, which were isolated from the natural and constructed wetlands, and the results of a batch test showed that P. stutzeri GIST-BDan2 (EF429003) completely oxidized in 1mM of As(III) to As(V) within 25-30h.
Abstract: Arsenic is subject to microbial interactions, which support a wide range of biogeochemical transformations of elements in natural environments such as wetlands. The arsenic detoxification potential of the bacterial strains was investigated with the arsenite oxidation gene, aox genotype, which were isolated from the natural and constructed wetlands. The isolates were able to grow in the presence of 10 mM of sodium arsenite (As(III) as NaAsO2) and 1 mM of d+glucose. Phylogenetic analysis based on 16S rRNA gene sequencing indicated that these isolated strains resembled members of the genus that have arsenic-resistant systems (Acinetobacter sp., Aeromonas sp., Agrobacterium sp., Comamonas sp., Enterobacter sp., Pantoea sp., and Pseudomonas sp.) with sequence similarities of 81–98%. One bacterial isolate identified as Pseudomonas stutzeri strain GIST-BDan2 (EF429003) showed the activity of arsenite oxidation and existence of aoxB and aoxR gene, which could play an important role in arsenite oxidation to arsenate. This reaction may be considered as arsenic detoxification process. The results of a batch test showed that P. stutzeri GIST-BDan2 (EF429003) completely oxidized in 1 mM of As(III) to As(V) within 25–30 h. In this study, microbial activity was evaluated to provide a better understanding of arsenic biogeochemical cycle in both natural and constructed wetlands, where ecological niches for microorganisms could be different, with a specific focus on arsenic oxidation/reduction and detoxification.
64 citations
TL;DR: It is suggested that dietary As(III)-induced urothelial cytotoxicity and proliferation are dose responsive, and the u rothelial effects have a threshold corresponding to the urinary excretion of measurable reactive metabolites.
64 citations
TL;DR: Histopathology of the gill indicates arsenite induced damage of the organ leading to its possible dysfunction and inhibition in the activities of glutathione-s-transferase (GST) and catalase (CAT) in the species indicate impairment of its vital detoxification process and elevated oxidative stress respectively.
54 citations
TL;DR: The results suggest that the repressive effect of NF-kappaB on p53 by mot-2 leads to genomic instability, which is involved in arsenite-induced malignant transformation of human keratinocytes.
52 citations
TL;DR: Coexposure of spleen cell cultures to PAHs and As(3)(+), both at individual low-effect concentrations, was found to produce profound suppression of the T-dependent antibody response (TDAR), demonstrating synergy between these two chemical classes of agents.
49 citations
TL;DR: Results suggest that roGFP2 is sensitive to redox potential change and thiol modification induced by environmental stressors, and provides a fast comprehensive detection system for toxicants that induce cellular oxidation.
Abstract: A highly specific, high throughput-amenable bacterial biosensor for chemically induced cellular oxidation was developed using constitutively expressed redox-sensitive green fluorescent protein roGFP2 in E. coli (E. coli-roGFP2). Disulfide formation between two key cysteine residues of roGFP2 was assessed using a double-wavelength ratiometric approach. This study demonstrates that only a few minutes were required to detect oxidation using E. coli-roGFP2, in contrast to conventional bacterial oxidative stress sensors. Cellular oxidation induced by hydrogen peroxide, menadione, sodium selenite, zinc pyrithione, triphenyltin and naphthalene became detectable after 10 seconds and reached the maxima between 80 to 210 seconds, contrary to Cd2+, Cu2+, Pb2+, Zn2+ and sodium arsenite, which induced the oxidation maximum immediately. The lowest observable effect concentrations (in ppm) were determined as 1.0 × 10−7 (arsenite), 1.0 × 10−4 (naphthalene), 1.0 × 10−4 (Cu2+), 3.8 × 10−4 (H2O2), 1.0 × 10−3 (Cd2+), 1.0 × 10−3 (Zn2+), 1.0 × 10−2 (menadione), 1.0 (triphenyltin), 1.56 (zinc pyrithione), 3.1 (selenite) and 6.3 (Pb2+), respectively. Heavy metal-induced oxidation showed unclear response patterns, whereas concentration-dependent sigmoid curves were observed for other compounds. In vivo GSH content and in vitro roGFP2 oxidation assays together with E. coli-roGFP2 results suggest that roGFP2 is sensitive to redox potential change and thiol modification induced by environmental stressors. Based on redox-sensitive technology, E. coli-roGFP2 provides a fast comprehensive detection system for toxicants that induce cellular oxidation.
TL;DR: Zinc can be beneficial against arsenic-induced hepatotoxicity in rats, and the zinc level and activities of SOD, GPx, GR, and CAT were found to be significantly increased following zinc treatment.
Abstract: The aim of present work was to gain insight into the role of dietary zinc in ameliorating the adverse effects caused by arsenic on rat liver. Male Wistar rats received arsenic alone in the form of sodium arsenite in drinking water at a dose level of 100 ppm, zinc alone in the form of zinc sulfate in drinking water at a dose level of 227 mg/L, or arsenic + zinc treatments in the combined group for a total duration of 3 months. Arsenic treatment resulted in a significant increase in lipid peroxidase (LPO); however, glutathione (GSH) levels and the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and catalase (CAT) were found to be significantly decreased following arsenic treatment. Furthermore, arsenic treatment resulted in a significant decrease in hepatic zinc levels. Histological studies showed well-differentiated signs of focal hepatitis, lobular inflammation, prominent hepatocyte degeneration, and severe periportal necrosis. Administration of zinc to arsenic-treated rats significantly decreased the level of LPO but increased the level of GSH compared with arsenic-treated rats. Further, the zinc level and activities of SOD, GPx, GR, and CAT were found to be significantly increased following zinc treatment. The administration of zinc to arsenic-treated rats caused signs of improvement in liver histoarchitecture, but a few focal areas of degeneration and necrosis were still occasionally seen. In conclusion, the results of this study suggest that zinc can be beneficial against arsenic-induced hepatotoxicity in rats.
TL;DR: Results suggested that Vicia/Allium root micronucleus (MN) assays are simple, efficient and reproducible methods for the genotoxicity monitoring of arsenic water contamination.
TL;DR: In vitro study suggested that ascorbic acid is helpful to ameliorate the arsenic-induced cytotoxicity and oxidative stress of rat hepatocytes and L-ascorbate also has potent cytoprotective role.
Abstract: Sodium arsenite-exposed hepatocytes of rat showed higher production of nitric oxide (NO) and increased lipid peroxidation (LPO) level vis-a-vis activity of superoxide dismutase (SOD) and catalase (CAT) were significantly lowered. Subsequently, the cell proliferation index (CPI) and cell viability were also reduced. Treatment with L-ascorbate was found effective in normalizing the arsenic-induced alteration of SOD and CAT activity and LPO level in rat hepatocytes. These observations indicated that L-ascorbate also has potent cytoprotective role as it could reduce the NO production and normalize the cell proliferation and viability of hepatocytes. Therefore, the in vitro study suggested that ascorbic acid is helpful to ameliorate the arsenic-induced cytotoxicity and oxidative stress of rat hepatocytes.
TL;DR: The ability of arsenite to induce autophagy in lymphoblastoid cell lines introduces a potentially novel mechanistic explanation of the well-characterized in vitro and in vivo toxicity of arsenic to lymphoid cells.
TL;DR: Arsenite is a major threat to female reproductive health acting as a reproductive toxicant and as an endocrine disruptor, restricted the function and structure of uterus, by altering the gonadotrophins and steroid levels, not only at high dose concentration but also at low levels, when they become mature.
TL;DR: The decrease in intracellular ROS and the increase in SOD2 and NQO1 expressions observed when HUVECs were treated with low concentration of NaAsO2, suggest the role of the two enzymes in protecting HUV ECs from injuries of arsenic exposure.
Abstract: To clarify the molecular mechanisms through which arsenic causes injuries to blood vessels, we analyzed the effects of sodium arsenite (NaAsO2) on the apoptosis of human umbilical vein endothelial cells (HUVECs), mitochondrial membrane potential (ΔΨm), intracellular reactive oxygen species (ROS), and the expression of the related genes. HUVECs apoptosis increased and ΔΨm decreased in a dose-dependent manner following arsenic treatment. Intracellular ROS showed 2 phase alterations: a slight decrease with low levels of arsenic (5 and 10 μM) treatment; but a sharp increase at higher concentrations (≧20 μM). The arsenic-induced cell apoptosis and intracellular ROS were blocked by the addition of the antioxidant N-acetyl-l-cysteine (NAC). The mRNAs of superoxide dismutase 2 (SOD2) and NAD(P)H:quinone oxidoreductase 1 (NQO1) increased strikingly when cells were treated with a low concentration of NaAsO2 (5 μM) and the level of induction was decreased with higher concentrations of arsenic treatment. Based on the results, we suggest that the decrease of ΔΨm caused by arsenic and the resulting cell apoptosis may contribute to the injuries of blood vessel in arsenism. The decrease in intracellular ROS and the increase in SOD2 and NQO1 expressions observed when HUVECs were treated with low concentration of NaAsO2, suggest the role of the two enzymes in protecting HUVECs from injuries of arsenic exposure.
TL;DR: Effective protection of gonadal weight loss, suppressed ovarian steroidogenesis, and altered ovarian and uterine peroxidase activities were noticed when 1.0 IU hCG/(100 g body weight day) is given in arsenic‐intoxicated rats.
Abstract: This study evaluated the involvement of hypophyseal-gonadal and hypophyseal-adrenal axes as a possible mechanism of sodium arsenite toxicity in ovary and uterus by the coadministration of hCG. Subchronic treatment of 0.4 ppm of sodium arsenite/(100 g body weight day) via drinking water for seven estrous cycles significantly suppressed the plasma levels of leutinizing hormone, follicle-stimulating hormone, and estradiol along with sluggish ovarian activities of Delta(5),3beta-hydroxysteroid dehydrogenase and 17beta-hydroxysteroid dehydrogenase followed by a reduction in gonadal tissue peroxidase activities in mature female rats at diestrous phase. Noticeable weight loss of the ovary and uterus along with prolonged diestrous phase and increased deposition of arsenic in the plasma and in these reproductive organs were also demonstrated following the ingestion of arsenic. Follicular atresia and thinning of the uterine luminal diameter were evident after sodium arsenite treatment. Effective protection of gonadal weight loss, suppressed ovarian steroidogenesis, and altered ovarian and uterine peroxidase activities were noticed when 1.0 IU hCG/(100 g body weight day) is given in arsenic-intoxicated rats. Normal estrous cyclicity was restored toward the control level after hCG coadministration, though the elimination of elementary arsenic from the plasma and gonadal tissues was impossible. A significant recovery in the restoration of ovarian and uterine histoarchitecture was prominent after hCG treatment. Adrenal hypertrophy and steroidogenic arrest of the adrenal gland along with altered level of brain monoamines in the midbrain and diencephalons following arsenic intoxication were also ameliorated after hCG coadministration.
TL;DR: In this article, the authors evaluated the ameliorative role of α-eleostearic acid and punicic acid, isomers of conjugated linolenic (CLnA) acid, against oxidative stress induced DNA damage.
TL;DR: It is demonstrated that dietary supplementation of antioxidants such as vitamins C and E could ameliorate arsenite induced toxicity in experimental rats.
Abstract: Serious health problems in humans are caused by arsenic-exposure, which is wide spread in the environment. Sodium arsenite, capable of inducing macromolecular damage is evaluated for its DNA damaging effect in the blood, liver, kidney and bone marrow cells of Wistar rats. Also the ameliorative potential of a-tocopherol (400 mg/kg body weight) and ascorbic acid (200 mg/kg body weight) supplemented orally to arsenic-intoxicated rats (100 ppm in drinking water for thirty days) in neutralizing the genotoxic effect of arsenite was explored. Detection of DNA damage at cellular level is evaluated by single cell gel electrophoresis or comet assay, under alkaline conditions. This study demonstrated that dietary supplementation of antioxidants such as vitamins C and E could ameliorate arsenite induced toxicity in experimental rats.
TL;DR: It is concluded that fenofibrate improves the integrity and function of vascular endothelium, and the vascular protecting potential of fen ofibrate in preventing the development of nicotine- and sodium arsenite-induced VED may be attributed to its additional properties such as activation of eNOS and generation of NO and consequent reduction in oxidative stress.
Abstract: The present study investigated the effect of fenofibrate, an agonist of PPAR-α, in nicotine- and sodium arsenite-induced vascular endothelial dysfunction (VED) in rats. Nicotine (2 mg/kg/day, i.p., 4 weeks) and sodium arsenite (1.5 mg/kg/day, i.p., 2 weeks) were administered to produce VED in rats. The scanning electron microscopy study in thoracic aorta revealed that administration of nicotine or sodium arsenite impaired the integrity of vascular endothelium. Further, administration of nicotine or sodium arsenite significantly decreased serum and aortic concentrations of nitrite/nitrate and subsequently reduced acetylcholine-induced endothelium-dependent relaxation. Moreover, nicotine or sodium arsenite produced oxidative stress by increasing serum thiobarbituric acid reactive substances (TBARS) and aortic superoxide generation. However, treatment with fenofibrate (30 mg/kg/day, p.o.) or atorvastatin (30 mg/kg/day p.o., a standard agent) significantly prevented nicotine- and sodium arsenite-induced VED and oxidative stress by improving the integrity of vascular endothelium, increasing the concentrations of serum and aortic nitrite/nitrate, enhancing the acetylcholine-induced endothelium-dependent relaxation and decreasing serum TBARS and aortic superoxide anion generation. Conversely, co-administration of L-NAME (25 mg/kg/day, i.p.), an inhibitor of nitric oxide synthase, markedly attenuated these vascular protective effects of fenofibrate. The administration of nicotine or sodium arsenite altered the lipid profile by increasing serum cholesterol and triglycerides and consequently decreasing high-density lipoprotein levels, which were significantly prevented by treatment with fenofibrate or atorvastatin. It may be concluded that fenofibrate improves the integrity and function of vascular endothelium, and the vascular protecting potential of fenofibrate in preventing the development of nicotine- and sodium arsenite-induced VED may be attributed to its additional properties (other than lipid lowering effect) such as activation of eNOS and generation of NO and consequent reduction in oxidative stress.
TL;DR: The hypothesis that tubular accumulation of As-Cu may have some bearing on the arsenic-associated nephrotoxicological process is supported.
Journal Article•
TL;DR: More pronounced nephrotoxic effects were noted in arsenic exposed diabetic group as evidenced by increased blood urea nitrogen, serum creatinine and relative kidney weight and decreased level of reduced glutathione and glutathion peroxidase activity compared to non arsenic exposure diabetic group.
Abstract: The present experiment was planned to study nephrotoxicity in experimental diabetic rats under sub-chronic exposure to arsenic. Alloxan induced diabetic and control rats were exposed to sodium arsenite (0 and 5.5 mg/kg, orally) for 30 days. More pronounced nephrotoxic effects were noted in arsenic exposed diabetic group as evidenced by increased blood urea nitrogen, serum creatinine and relative kidney weight and decreased level of reduced glutathione and glutathione peroxidase activity compared to non arsenic exposed diabetic group. Increased level of lipid peroxidation, protein oxidation, superoxide dismutase and catalase activities under diabetic condition remained unchanged in arsenic exposed diabetic group compared to unexposed diabetic group.
TL;DR: The results demonstrated that exposure to low concentration arsenite enhanced BEAS-2B cells growth and cyclin D1 mRNA and protein expression and demonstrated that the non-canonical NF-kappaB pathway was involved in arsenite-induced cyclinD1 expression.
TL;DR: It is hypothesized that arsenic plus iron synergistically induces hepatic damage mediated through oxidative stress in rats, which indicates an important public health issue: using iron precipitants to remove arsenic from water may cause oxidative hepaticDamage in humans.
TL;DR: It is concluded that benfotiamine reduces oxidative stress and activates endothelial nitric oxide synthase to enhance the generation and bioavailability of NO and subsequently improves the integrity of vascular endothelium to prevent sodium arsenite-induced experimental VED.
Abstract: The present study has been designed to investigate the effect of benfotiamine, a thiamine derivative, in sodium arsenite-induced vascular endothelial dysfunction (VED) in rats. Sodium arsenite (1.5 mg−1 kg−1 day−1 i.p., 2 weeks) was administered in rats to produce VED. The development of VED was assessed by employing isolated aortic ring preparation and estimating the serum and aortic concentrations of nitrite/nitrate. Further, the integrity of vascular endothelium in thoracic aorta was assessed by scanning electron microscopy. Moreover, the oxidative stress was assessed by estimating serum thiobarbituric acid reactive substances (TBARS) and aortic superoxide anion generation. The administration of sodium arsenite markedly produced VED by attenuating acetylcholine-induced endothelium-dependent relaxation, decreasing serum and aortic concentrations of nitrite/nitrate, and impairing the integrity of vascular endothelium. Further, sodium arsenite produced oxidative stress by increasing serum TBARS and aortic superoxide generation. The treatment with benfotiamine (25, 50, and 100 mg−1 kg−1 day−1 p.o.) or atorvastatin (30 mg−1 kg−1 day−1 p.o., a standard agent) prevented sodium arsenite-induced VED and oxidative stress. However, the beneficial effects of benfotiamine in preventing the sodium arsenite-induced VED were attenuated by co-administration with N-omega-nitro-l-arginine methyl ester (L-NAME) (25 mg−1 kg−1 day−1, i.p.), an inhibitor of NOS. Thus, it may be concluded that benfotiamine reduces oxidative stress and activates endothelial nitric oxide synthase to enhance the generation and bioavailability of NO and subsequently improves the integrity of vascular endothelium to prevent sodium arsenite-induced experimental VED.
TL;DR: It is highlighted that co-administration of GSH could ameliorate arsenic-mediated injuries of female reproductive organs as well as tissue deposition of arsenic appeared to be unaffected by dietary GSH.
TL;DR: The increased transcription of AQP9 has been observed in fasting and diabetic rats, suggesting that this channel could play a role in the diabetogenic effect of arsenic.
TL;DR: It may be concluded that rosiglitazone reduces oxidative stress, activates eNOS and enhances the generation of nitric oxide to prevent sodium arsenite-induced VED in rats.
Abstract: The present study has been designed to investigate the effect of rosiglitazone, a peroxisome proliferator activated receptor γ agonist in sodium arsenite-induced vascular endothelial dysfunction (VED) in rats. The rats were administered sodium arsenite (1.5 mg/kg/day, i.p., 2 weeks) to induce VED. The development of VED was assessed by employing isolated aortic ring preparation and estimating serum nitrite/nitrate concentration. Further, the integrity of the aortic endothelium was assessed histologically using haematoxylin-eosin staining. Moreover, the oxidative stress was assessed by estimating serum thiobarbituric acid reactive substances, aortic reactive oxygen species and reduced form of glutathione. The administration of sodium arsenite produced VED by impairing acetylcholine-induced endothelium dependent relaxation, diminishing the integrity of vascular endothelium and decreasing the serum nitrite/nitrate concentration. In addition, sodium arsenite was noted to produce oxidative stress as it increased serum thiobarbituric acid reactive substances and aortic reactive oxygen species and consequently decreased glutathione. Treatment with rosiglitazone (3 mg/kg/day, p.o., 2 weeks and 5 mg/kg/day, p.o., 2 weeks) significantly prevented sodium arsenite-induced VED by enhancing acetylcholine-induced endothelium dependent relaxation, improving the integrity of vascular endothelium, increasing the nitrite/nitrate concentration and decreasing the oxidative stress. However, the vascular protective effect of rosiglitazone was markedly abolished by co-administration of nitric oxide synthase inhibitor, N-Omega-Nitro-L-Arginine Methyl Ester (L-NAME) (25 mg/kg/day, i.p., 2 weeks). Thus, it may be concluded that rosiglitazone reduces oxidative stress, activates eNOS and enhances the generation of nitric oxide to prevent sodium arsenite-induced VED in rats.
TL;DR: Results indicate that the tannin-rich green tea could have improved the defense mechanism against arsenic-induced oxidative stress and reduced the tissue arsenic burden.
Abstract: The protective effect of green tea (Camellia sinensis) was tested against arsenic-induced toxicity. However, the possible role of tannins in green tea in alleviating hepatic and renal oxidative injury has also been studied. Administration of sodium arsenite (100 mg/kg/day) for 28 days in Sprague Dawley female rats resulted in significant reduction of biochemical parameters such as delta-aminolevulinic acid dehydratase (ALAD), reduced glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD) and elevation of thiobarbituric acid reactive substances (TBARS) and the index of nitrite/nitrate (NOx) levels. The tissue arsenic burden was increased after arsenic exposure for a period of 28 days. Green tea crude fraction (GTC) co-treated with sodium arsenite for 28 days caused significant (p < .01) elevation of ALAD, GSH, GPx, SOD, and nitrate/nitrite levels and reduction of the TBARS level and tissue burden when compared to detannified green tea fraction (GTDT)-treated groups. The protective role of tannin-rich fraction of C. sinensis when compared to the detannified fraction was also confirmed by histological examinations. The greater activity of GTC than that of detannified green tea fraction correlates with the higher content of tannins in green tea. Overall, these results indicate that the tannin-rich green tea could have improved the defense mechanism against arsenic-induced oxidative stress and reduced the tissue arsenic burden.