Showing papers on "Lead acetate published in 2006"
TL;DR: Macha prevented LA-induced spermatogenic disruption in rats and it may become in a potential treatment of male infertility associated with lead exposure, according to a study of rats treated with or without Maca.
90 citations
TL;DR: It is demonstrated that both lead and cadmium caused a significant reduction in gonadotropin binding, which altered steroidogenic enzyme activity of granulosa cells, which exhibited a positive correlation with membrane changes of the granul Rosa cells.
69 citations
TL;DR: The combination treatment with thiamine and ascorbic acid at lower doses effectively inhibited testicular cells from apoptosis by lead acetate, but higher doses could aggravate the testicular lesion.
61 citations
TL;DR: It can be hypothesized that glycyrrhizin is a potent chemopreventive compound against lead acetate mediated hepatic oxidative stress, toxicity and tumor promotion related responses in rats.
60 citations
TL;DR: Turmeric and myrrh are useful herbal remedies, especially for controlling oxidative damages and genotoxicity induced by lead acetate intoxication, and the powerful protection was observed with 5% powdered turmeric.
Abstract: The effects of lead acetate in the diet (05% w/w) on reduced GSH, activity of phase II metabolizing enzyme glutathione S-transferase (GST), lipid peroxidation in liver homogenate and bone marrow chromosomes of mice simultaneously supplemented with powdered turmeric and myrrh for 8 weeks were investigated Five groups of Swiss male albino mice, each of 30 mice, the first group received a basal diet and served as negative control, the second group received basal diet supplemented with lead acetate only and served as positive control The other three groups received basal diet supplemented with lead acetate and 1% or 5% turmeric powder and 1% myrrh powder, respectively Results revealed a significant decrease in the amount of GSH in all treated groups compared with negative control Also, the activity of GSH S-transferase was significantly decreased in positive control compared with other groups However, co-administration of the protective plants resulted in a significant increase in the activity of GST compared with both positive and negative control groups Furthermore, lipid peroxidation was significantly increased in positive control alone, while cotreatment with the protective plants resulted in reduction in the level of lipid peroxidation by 31% and 49% in mice receiving 1% and 5% turmeric powder respectively and 45% in 1% myrrh treated when compared with their respective positive control group Lead genotoxicity was confirmed through significant reduction in the number of dividing cells, increased total number of aberrant cells and increased frequency of chromosomal aberrations Simultaneous treatment with these plants significantly reduced the genotoxicity induced by lead administration and the powerful protection was observed with 5% powdered turmeric It may be concluded that turmeric and myrrh are useful herbal remedies, especially for controlling oxidative damages and genotoxicity induced by lead acetate intoxication
54 citations
TL;DR: The present study reports a definite synergistic trend of immunotoxicity during simultaneous exposure to arsenic and lead, that is, a multimetal challenge, as compared to the effects of independent exposure to them.
38 citations
TL;DR: It is suggested that lead could modulate the immune system by targeting the humoral as well as innate immune cells.
Abstract: Metal toxicants may affect immune regulation with an increased incidence of infectious diseases, cancer or autoimmune diseases. Lead is the leading environmental toxin among heavy metals and has aroused concern, as continuous low-level exposure leads to a variety of health problems. We compared serum immunoglobulins (Ig) and reactive oxygen and nitrogen intermediates (super oxide and nitric oxide (NO)) in culture supernatant of lead-exposed (blood lead; Pb-B > 10 microg/dL) individuals with that of unexposed healthy controls (blood lead < 10 microg/dL). The serum IgA level was significantly increased in lead-exposed individuals in comparison to controls (182 +/- 53 versus 138 +/- 52 mg/dL; P < 0.05). Furthermore, lipopolysaccharide-induced NO production by mouse macrophage cells, RAW 264.7, showed significant suppression (P < 0.05) after treatment with lead acetate (100 ppm). This study suggested that lead could modulate the immune system by targeting the humoral as well as innate immune cells.
34 citations
TL;DR: Investigation of the ultrastructural effects of lead on the brain of rats found vacularisation of cell cytoplasm and degeneration in mitochondria, in the perinuclear cy toplasm, electron-dense inclusion bodies were detected, and dilation were in the endopasmic reticulum.
Abstract: Lead is a metal that has been implicated in toxic processes, which affect several organ systems in humans and other animals. The purpose of this study was to investigate the ultrastructural effects of lead on the brain of rats.Wistar Albino rats (180-200 g body weight) were divided into a controlled and lead acetate-exposed group. Rats received lead acetate at 500 ppm in their drinking water for 60 days. Both groups were fed with the same standard food, but lead acetate was added to the drinking water. During the experimental period, blood samples were drawn from the abdominal aorta of the anesthetised animals. At the end of exposure, body weight and blood lead levels were measured. The brain tissue samples were preapared and analysed by light and transmission electron microscopy. In the brain cortex, degeneration in some of the neuron cells, in the lumens of the blood vessels, dilation, hemorhagia and free floating erytrocytes were observed. Ultrastructural changes were revealed in the form of vacularisation of cell cytoplasm and degeneration in mitochondria, in the perinuclear cytoplasm, electron-dense inclusion bodies were detected, and dilation were in the endopasmic reticulum.
34 citations
TL;DR: The concept that a long-term chronic exposure to Pb induced alterations upon some morphophysiological and genetic paramaters in Algerian mice is supported.
Abstract: Time-dependent effects of lead (Pb) toxicity were studied in Algerian mice (Mus spretus) treated with Pb acetate via drinking water (1 g Pb acetate/L) for different periods of exposure (15, 45, and 90 d). End points included the determination of hepatic Pb concentration and the assessment of some morphophysiological, biochemical and cytogenetical parameters. A control group receiving distilled water was also monitored for comparative purposes. Hepatic Pb accumulation increased with the time of exposure and was significantly higher in treated mice when compared to controls. In association with significant body mass loss in Pb-exposed mice, for 15 and 45 d, a significant increase in the relative spleen mass was observed after 45 d of intoxication. Pb-exposed mice also showed significant decreases in red blood cells, hematocrit, and mean corpuscular hemoglobin. On the contrary, changes in plasma transferases (aspartate aminotransferase and alanine aminotransferase) and hepatic superoxide dismutase activities did not reach statistical significance. A significant increase in the frequency of micronucleated polychromatic bone marrow erythrocytes was also found in the 90-d-exposed mice, compared to nontreated mice and the other exposed groups. Exposure to Pb acetate resulted also in a slight time-dependent decrease of the polychromatic-normochromatic ratio. These results support the concept that a long-term chronic exposure to Pb induced alterations upon some morphophysiological and genetic parameters in Algerian mice.
30 citations
TL;DR: It is concluded that vascular adrenergic system and nitric oxide pathway change in short-term and subchronic phases of lead poisoning.
29 citations
TL;DR: The present work indicates that it is possible to evaluate the ERK1/2 and p38(MAPK) activation in the central nervous system (CNS) of a freshwater fish largely distributed in South America.
TL;DR: The results suggest that calcium pectate and calcium alginate may be considered perspective dietary compounds purposed for prevention and treatment of chronic lead poisoning.
Abstract: Exposure to environmental lead remains a widespread problem in most industrialized countries. Usage of modern agents purposed for elimination of heavy metals as well as for therapy and prevention of chronic poisoning does frequently result in toxic signs. Dietary nonstarch polysaccharides were suggested to be effective when used for this purpose. The present study was conducted to estimate metal binding capacity and effects of calcium salts of pectate and alginate on lead absorption, distribution, and removal with feces. Under in vitro conditions calcium alginate showed the highest lead-binding capacity in comparison with other agents studied. Metal binding capacity of calcium pectate was slightly lower. In rats simultaneous administration of lead acetate and suspensions containing calcium alginate or calcium pectate prevented metal absorption and significantly reduced lead accumulation in inner organs and femur. In experiments estimating lead removal from inner organs and femur in rats preliminary exposed to the heavy metal, calcium alginate and calcium pectate were the most effective agents studied in comparison with others, as indicated by reduced lead concentration in organs and femur as well as increased metal content in feces of laboratory animals. The results suggest that calcium pectate and calcium alginate may be considered perspective dietary compounds purposed for prevention and treatment of chronic lead poisoning.
TL;DR: It is suggested that early post-natal lead exposure induces persistent changes in the number of PSA-NCAM expressing cells, which could be, at least, partly the basis of impairments in the learning and memory formation, which follows low-level lead exposure.
Abstract: Although lead is widely known as a potent neurotoxin, the effect of lead exposure on the expression of the polysialic acid linked neural cell adhesion molecule (PSA-NCAM) remains unclear. We exposed Wistar rat pups to 0.2% lead acetate from postnatal day (PND) 1 to PND 30. This exposure protocol resulted in pup blood lead levels, which increased to 29.3 ± 5.0 mg/dl on PND 15, and subsequently rose to 34.2 ± 5.8 mg/dl at weaning. Corresponding brain tissue lead levels were 456 ± 23 ng/g on PND 15 and 781 ± 87 ng/g on PND 30. Animals were sacrificed on PND 80, when the blood and brain lead concentrations did not differ from those of the control group. Lead exposure induced a significant increase in the total number of PSA-NCAM expressing cells, compared to the control group ( p
TL;DR: The number of total red blood cells showed a tendency to decrease after the injections of the metal, whereas the number of white blood cells (WBC) increased significantly; the differential leukocyte counts showed a statistically significant increase in the absolute number and in the relative percentage of blast-like cells.
Abstract: Lead is a multiple-source pollutant, well known for its toxicity, of great risk both for the environment and human health. The main target organs of lead are the hematopoietic, nervous, and renal systems; there are also reports in support of its impairment effects on the reproductive and immune systems. It is well known that most of the metal is accumulated in the blood cells and that many of the deleterious effects are related to its circulating concentrations. These adverse effects have been described not only in humans but also in a number of other vertebrates such as fish and birds. The purpose of the present work was to evaluate the effects of weekly administration of sublethal Pb (as acetate, 50 mg ċ kg−1) during 6 weeks on the profile of the serum proteins and blood cell counts of the adult South American toad, Bufo arenarum (Anura: Bufonidae). The electrophoretic patterns of serum proteins pointed out the presence of four fractions; the metal provoked a significant decrease in both total proteins and albumin fraction; among the globulin fractions, the G3 resulted augmented. These findings may be related to the impact of lead on the toads’ hepatic cells and immune system. The number of total red blood cells (RBC) showed a tendency to decrease after the injections of the metal, whereas the number of white blood cells (WBC) increased significantly; the differential leukocyte counts showed a statistically significant increase in the absolute number and in the relative percentage of blast-like cells. The decrease in RBC was attributed to the negative impact of the metals on the hemoglobin synthesis. The increasing of the WBC counts may be interpreted as a consequence of the induction of proliferation of pluripotential hematopoietic cells.
TL;DR: A significant change in the levels of various antioxidative enzymes and serum albumin as well as total protein contents of protein-deficient rats subjected to lead treatment was indicated and zinc supplementation has tended to normalize the altered levels of these enzymes to a significant extent.
Abstract: The current study was designed to evaluate the hepatoprotective role of zinc after lead (Pb) treatment of protein-deficient (PD) rats. The animals were subjected to seven different treatment groups: G-1 (normal control, 18% protein), G-2 (protein-deficient, 8% protein), G-3 (Pb-treated, 100 mg/kg body weight of lead acetate), G-4 (Zn-treated, zinc sulfate at a dose level of 227 mg/L drinking water), G-5 (PD + Pb-treated), G-6 (PD + Zn-treated), and G-7 (PD + Pb + Zn-treated). Serum albumin levels and total serum protein contents were estimated to assess the severity of protein deficiency at the end of 8 weeks in all the treatment groups. Also, the study explored the role of zinc on antioxidative defense system enzymes in liver of protein-deficient rats subjected to lead toxicity treatment. Further, the study was extended to elucidate the levels of zinc and lead in liver tissue after different treatments of rats using positron-induced X-ray emission technique (PIXE). The current study indicated a significant change in the levels of various antioxidative enzymes and serum albumin as well as total protein contents of protein-deficient rats subjected to lead treatment. A significant increase in the levels of malondialdehyde (MDA), catalase, and glutathione peroxidase (GPx) was seen after 8 weeks of lead treatment of protein-deficient rats. On the contrary, levels of albumin, total protein content, superoxide dismutase (SOD), GSH, were found to be decreased. Interestingly, zinc supplementation has tended to normalize the altered levels of these enzymes to a significant extent. The levels of zinc in liver tissue was found to be decreased significantly in protein-deficient as well as lead-treated rats. However, hepatic zinc concentration was increased to a significant extent in protein-deficient rats supplemented with zinc when compared with protein-deficient rats. Further, the presence of lead was also observed in livers of lead-treated animals. In conclusion, the study revealed the antioxidative role of zinc in hepatotoxic conditions induced by subjecting the rats to protein-deficient diet and lead treatment.
TL;DR: There is synergistic antioxidative effect between Vit C and Vit E that protects the liver from lead induced lipid peroxidation, suggesting that the antioxidant treatment may best be done using a balanced cocktail.
Abstract: Introduction: Oxidative stress with subsequent lipid peroxidation has been postulated as
one mechanism for lead toxicity. The protective action of vitamins C and E against lead affects lipid hydroperoxide level and liver functions in male rats has been studied.
Results: Administration of lead acetate (2%) in dirinking water for 3 months elevates plasma lipid hydroperoxide level, activities of aspartate aminotronsferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP), cholesterol, triglycerides and low density lipoprotein (LDL) levels. On the other hand, reduced plasma glutathione (GSH), protein and high density lipoprotein (HDL) concentrations lowered significantly in lead (Pb) treated group. However, oral administration of vitamin C (Vit C) or vitamin E (Vit E) at dose level of 100 mg/kg body weight reduced the alterations in the previous parameters. On the other hand, co-administration of both vitamins (Vit C+ Vit E) to lead-treated rats led to the most significant decline in lipid hydroperoxide level, restoration of GSH level and exhibited more protection as compared with Vit C or Vit E separately.
Conclusion: There is synergistic antioxidative effect between Vit C and Vit E that protects the liver from lead induced lipid peroxidation, suggesting that the antioxidant treatment may best be done using a balanced cocktail. .
TL;DR: This in vitro study confirms the existence of oxidative stress due to lead exposure and suggests that SeCys can confer protection against lead-induced toxicity in CHO cells and neurotoxicity in PC-12 cells.
TL;DR: The results show that morphological changes in rat brain are correlated with increased lipid peroxidation, and the lead levels of the umbilical cord, however it is not clear whether oxidative stress is the cause or the consequence of these neurotoxic effects of lead.
Abstract: The effect of prenatal lead acetate exposure was studied microscopically together with the concentration of lead and lipid fluorescent products (LFP) in the brain of rat fetuses. Wistar rats were intoxicated with a lead solution containing either 160 or 320 ppm of lead acetate solution during 21 days through drinking water. The control group (ten rats) received deionized water for the same period. The rats were killed on gestation day 21 and fetuses were obtained; the placenta, umbilical cord and parietal cortex (Cx), striatum (St), thalamus (Th) and cerebellum (Ce) were collected for measuring tissue lead concentration, LFP as an index of lipid peroxidation and histopathologic examination. Lead contents were increased in placenta, umbilical cord, St, Th and Cx in both lead-exposed groups. Lead exposure increased (LFP) in placenta and umbilical cord, St, Th and Ce as compared to the control group. Histopathological examination showed severe vascular congestion in placenta, the Cx, St, Th and Ce with hyperchromatic and shrunken cells. Interstitial oedema was found in all regions studied of both lead exposed groups. The morphometric evaluation of the studied brain regions showed an absolute decrease in total cell number and increased number of damaged cells and interstitial oedema. Our results show that morphological changes in rat brain are correlated with increased lipid peroxidation, and the lead levels of the umbilical cord, however it is not clear whether oxidative stress is the cause or the consequence of these neurotoxic effects of lead.
TL;DR: A dose-dependent effect on reproduction is indicated, with variations in the number of births and in pups' weight, at the weaning stage, with hemoglobin levels and erythrocyte numbers significantly decreased.
Abstract: The effects of exposure to high doses of lead on reproduction and development have been established, but not so those caused by low lead doses or the influence that life stage at which contact with the metal takes place might have. The aim of this work was to study the effects of 200 and 400 ppm lead acetate in drinking water on reproduction and development as well as on renal and hepatic parameters of rats at different life stages, from gestation to 3 mo postweaning. The results indicate a dose-dependent effect on reproduction, with variations in the number of births and in pups' weight. Development was mostly affected at the weaning stage, with hemoglobin levels and erythrocyte numbers significantly decreased. The lead levels in tissues, blood, urine, and feces along with selected renal and hepatic parameters (blood urea nitrogen, creatinine, alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase) were determined. There were histological, blood urea nitrogen, alanine aminotransferase, and alkaline phosphatase changes in the first month postweaning. After 3 mo, these changes are no longer evident, possibly because of metabolic adaptation.
TL;DR: Examining Brn-3a protein and RNA expression in rat brain following low-level lead exposure during development and subsequent effects on spatial learning and memory suggests that the alteration of Brn -3a may play a key role in the mechanisms underlying lead neurotoxicity.
TL;DR: In fact, BAL and DMPS increase the inhibitory effect of lead on delta-ALA-D activity from mice blood, and the complexes formed were more inhibitory than lead alone in kidney and liver enzyme activity, ex vivo.
01 Jan 2006
TL;DR: It was observed that ascorbic acid treatment prior to lead intoxication reduced the depletion in the normal hepatocytes count and the elevation in binucleate as well as abnormal hepatocytes in comparison to their respective control.
Abstract: Summary The objective of this study was to screen for the hepatoprotective role of ascorbic acid (vitamin C) against lead acetate intoxication in mice. For this purpose, animals were randomized into control and experiment groups. Mice of the experimental group were administered ascorbic acid (400 mg/kg of body weight/ animal) orally once in a day for 7 consecutive days. Animals were then treated with lead acetate (intraperitoneally) on 7 th day, one hour after ascorbic acid administration. These were then autopsied at various post-treatment intervals (6 hrs to 20 days) to examine quantitative as well as qualitative alterations in the liver. Results from the present investigation reveal a certain degree of histopathological and biochemical alterations caused by lead due to impaired oxidantantioxidant balance and enhanced oxidative stress. It was observed that ascorbic acid treatment prior to lead intoxication reduced the depletion in the normal hepatocytes count and the elevation in binucleate as well as abnormal hepatocytes in comparison to their respective control. Also, supplementation of ascorbic acid ameliorated the biochemical alterations i.e., glycogen, cholesterol and protein, in the liver of mice. A fall in glutathione level was noted in blood and liver in mice; whereas administration of Vitamin C significantly (p<0.05) reduced the level of glutathione in the Vitamin C treated experimental group as compared to the control.
TL;DR: Oct-2 is identified as a potential molecular target for Pb and it is suggested that Oct-2 may be associated with lead-induced disturbances in gene expression, and developmental maintenance of Sept-2 DNA binding could be impacted through de novo synthesis.
TL;DR: In this article, the effect of lead acetate trihydrate on platinum black coating was examined for the electrolyte free of or including lead acetates using cyclic potential-current curves and a multi-pulse current measurement.
Abstract: The effect of lead acetate trihydrate on platinum black coating has been examined for the electrolyte free of or including lead acetate trihydrate using cyclic potential–current curves and a multi-pulse current measurement. The current–potential curves measured with a cyclic sweep of a current density in the electrolyte including lead acetate trihydrate show that no peak assigned to the reduction of Pt (IV) to Pt (II) in the process of electrode reactions is observed. The kinetic constant, the exchange current density and the double-layer capacitance, which can be determined from the measured potential–time curves, exhibit significantly different values for H 2 PtCl 6 electrolytes free of or containing lead acetate trihydrate. In particular, the exchange current density for the electrolyte including lead acetate trihydrate is much larger than that for the electrolyte free of lead acetate trihydrate. These experimental results indicate that lead acetate trihydrate significantly enhances the electrode reactions in platinum black coating by mainly lowering a height of the energy barrier for the reduction of Pt (IV) to Pt (0) and by suppressing the reduction of Pt (IV) to Pt (II).
TL;DR: In this paper, a trimer structure of lead glycolate was identified based on high-resolution mass spectroscopy, chemical analysis composition, FTIR, 13 C-solid state NMR and TGA.
Journal Article•
TL;DR: Activated charcoal may protect the lead-induced toxicity on kidney and reduce the increase of serum BUN and Creatinine level induced by lead.
Abstract: A protective effect of activated charcoal against the acute lead poisoning of kidney was studied in mice. Mice approximately 30 gm in weight were grouped into the control, lead acetate-treated. and the activated charcoal-treated after lead acetate groups. Lead acetate (60mg/kg) and activated charcoal (40mg/kg) were delivered orally. Serum BUN and creatine were measured and ultrastructural alteration of renal tissues were examined by electron microscopy. Activated charcoal were decreased the increase of serum BUN and Creatinine level induced by lead. Lead acetate-treated renal tissues were characterized by the loss of microvilli in the renal tubule tells, irregular nucleus, enlarged and reduced number of mitochodria, enlarged rough endoplasmic reticulum, loss of ribosomes. Cells treated with activated charcoal were similar to those of the control group. In conclusion, activated charcoal may protect the lead-induced toxicity on kidney.
Journal Article•
TL;DR: It is suggested that testosterone supplementation in lead-treated rats protects adrenocortical activity and testicular spermatogenesis and lead acetate administration resulted in a significant increase in adrenal steroidogenic enzyme and serum levels of corticosterone.
Abstract: The potential health hazard of the large amounts of Lead that occurs in canned baby food, domestic water from lead-lined tanks and, in printing and petroleum industries. Lead acetate administration at a does of 8 mg/kg body weight for 21 days resulted a significant increase in adrenal steroidogenic enzyme (Delta5-3beta- HSD) and serum levels of corticosterone, while serum levels of testosterone, FSH, LH and testicular spermatogenesis were decreased in albino rats. But lead-treated rats received exogenous testosterone for the last 14 days of lead treatment, showed prevention of adrenocortical hyperactivity by decreasing adrenal Delta5-3beta-HSD activity and serum level of corticosterone. Testosterone administration also increased serum level of testosterone, FSH and LH along with spermatogenesis. The results suggest that testosterone supplementation in lead-treated rats protects adrenocortical activity and testicular spermatogenesis.
Journal Article•
TL;DR: In this paper, the prophylactic efficacy of garlic (Allium sativum) to reduce tissue lead (Pb) concentration was evaluated experimentally in Iran's crossbred Iranian female goats.
Abstract: The prophylactic efficacy of garlic (Allium sativum) to reduce tissue lead (Pb) concentration was evaluated experimentally in goats. Eight crossbred Iranian female goats were divided into two equal groups. Goats of group A received lead acetate orally at the dose rate of 80 mg/kg BW and group B received concurrent lead acetate orally at the dose rate of 80 mg/kg BW and dried garlic powder orally at the dose rate of 45 g/animal/day for 5 days. Mean serum lead concentration in group A goats was 0.13 ± 0.03 µg/ml before lead administration and 0.56 ± 0.04 µg/ml on 5th day, whereas in group B the concentration was 0.11 ± 0.02 µg/ml before treatment and 0.29 ± 0.02 µg/ml on the 5th day. Mean urine lead concentration in group A ranged between 0.05 ± 0.02 µg/ml before lead administration and 0.45 ± 0.07 µg/ml on the 5th day, whereas in group B it was 0.07 ± 0.01 µg/ml before treatment and 4.08 ± 0.93 µg/ml on the 5th day. The mean lead concentrations in bones, lungs, heart, liver, kidneys and skeletal muscles of group A following necropsy were 39.95 ± 6.94, 0.65 ± 0.06, 0.46 ± 0.07, 6.61 ± 0.74, 19.32 ± 2.17, 0.27 ± 0.06 µg/g of wet tissue, respectively. The respective values in group B were 17.77 ± 4.12, 0.20 ± 0.04, 0.20 ± 0.02, 1.45 ± 0.30, 2.37 ± 0.27 and 0.11 ± 0.01 µg/g of wet tissue. Thus, concurrent use of lead acetate and garlic dry powder reduced lead concentration considerably, indicating the potential activity of garlic against lead toxicity in goats.
Journal Article•
TL;DR: Thiamine and ascorbic acid could antagonize the action of certain toxicity of testes in mice treated by lead acetate and promote testicular cell apoptosis via elevated expression of TGFP, and Caspase-3.
Abstract: OBJECTIVE: To investigate the impacts of the combined administration of ascorbic acid and thiamine on certain biochemical and morphologic indexes of testes in mice exposed to lead. METHOD: s 75 male mice were divided into control groups, groups received with 0.2% lead acetate and groups treated by the same lead acetate dose in combination with ascorbic acid and thiamine (subdivided into:low, middle and high-dose) ad libitum with 15 mice in each. 5 mice in each group were sacrificed at 2, 4 and 6 weeks respectively, and then testes were separated from mice. To evaluate the lead toxicity in testis, the levels of TGFbeta1 and Caspase-3 were detected by immunohistochemistry, apoptotic cell was determined by terminal deoxynucleotidyl transferase (TdT) mediated dUTP nick end labeling (TUNEL); DNA damage of germ cells was assessed by single cell gel electrophoresis (SCGE or Comet assay). RESULTS: The levels of TGFbeta1 and Caspase-3, apoptotic index were significantly higher in groups given by lead than those in control groups( P < 0.05 ). After intervention of low and middle-dose vitamins, DNA damage and the number of apoptotic cell in testis were obviously lower than those of groups exposed to lead( P < 0.05 ) . Also, the impaired tissues were markedly ameliorated under light microscope. Groups administrated with vitamins at the highest dose, however, promoted testicular cell apoptosis via elevated expression of TGFP, and Caspase-3, percentage of tail cell and tail length were reduced significantly. CONCLUSION: Thiamine and ascorbic acid could antagonize the action of certain toxicity of testes in mice treated by lead acetate.
TL;DR: Lead exposure during different gestation periods should have a traumatic effect on the trophoblast, leading to interference of nutrition and oxygen exchange and reduction of placenta weight and retardation of development of pups.
Abstract: OBJECTIVE To investigate the effects of lead exposure to rat placenta and pups during different gestation periods METHODS All 108 Wistar rats (72 females, 36 males) were randomly divided into four groups All rats were orally fed with 0025% lead acetate during different gestation periods Blood was obtained from the abdominal vena cava and the lead level in maternal blood was measured by means of atomic absorption spectrometry at the end of the pregnancy The number of pups, their body weight, body length and tail length were measured The effects of lead to rat placenta were observed by level of microscopy, optical microscopy and electronic microscopy RESULTS Experimental groups the blood lead level at the end of gestation were above 0483 micromol/L There were significant differences among, of pups, during different groups (P < 001) Among them the drinking lead group of whole distant was the lowest in placenta weight [(031 +/- 013) g] body weight of pups [(208 +/- 088) g] length and tail length of pups [(237 +/- 032) cm, (098 +/- 009) cm] There were significantly differences between the experimental groups and controls Maternal blood lead level was negatively related to placenta weight (r = 0652, P < 001), and had no relation with the body weight of pups (r = -0107, P = 046) In the experimental groups of lead poisoned rats, the placenta showed focus necrosis in the deciduas, and increased the trophoblastic giant cells and light staining cells in the trophospongium Trophoblast in the labyrinth and trophospongium showed degeneration; fibrin deposition around the villi was increased Microvilli around the trophoblast were shorter and less, mitochondrion was swollen and decreased in number, rough endoplasmic reticulum was distended and ribosomal number on membrane decreased CONCLUSION Lead exposure during different gestation periods should have a traumatic effect on the trophoblast, leading to interference of nutrition and oxygen exchange Furthermore, the blood supply to the placenta and nutrition and oxygen exchange between mother and pups were also interfered, leading to reduction of placenta weight and retardation of development of pups