Ameliorative Effect Of Vitamin Research Articles

Ameliorative effect of vitamin E on trichloroethylene-induced nephrotoxicity in rats.

Background: 1,1,2-Trichloroethylene (TCE) is an important organic solvent which is widespread in the environment. Work place exposure to TCE has been associated adverse effects in many organs including kidney. Vitamin E is an antioxidant that can overcome oxidative stress. Objectives: The aim of the present study is to examine the role of vitamin E against destructive effects of TCE on rat kidney. Materials and Methods: A total of 35 male Wistar rats were randomly divided into seven groups of equal number in each. The rats in group I were the controls received vehicle only. Animals in groups III, V and VII received intraperitoneal injection (i.p) of corn oil. Rats in groups of II, IV, and VI were received vitamin E at a dose of 200 mg/kg; 30 minutes later, animals were received TCE (i.p) at doses of 1000 mg/kg (groups II and III), 1500 mg/kg (groups of IV and V), and 2000 mg/kg (groups of VI and VII) respectively. The experiment repeated for 7 consecutive days. Twenty-four hours after last administration, animals were killed with overdose of sodium pentobarbital. Blood samples were analyzed for blood urea nitrogen (BUN) and creatinine (Cr). One part of the kidney tissues were excised for measuring malondialdehyde (MDA) and glutathione (GSH) concentrations. Another part were excised for histopathological estimation. Results: TCE induced a dose-dependent elevation in BUN, Cr, MDA and markedly decreased GSH level when compared to those in control rats. TCE-induced dose-dependent injury in rat kidney tissue. Vitamin E significantly decreased BUN, Cr, MDA and increased GSH levels and protected kidney damage in TCE treated animals. Conclusions: The observations suggest that vitamin E may have a protective effect against TCE-induced oxidative stress in the rat kidney.

Ameliorative Effect of Vitamin E on Oxidative Stress Induced by Bisphenol A in Female Albino Rats

Objective: Oxidative stress is induced by bisphenol A (BPA) and affects many organs. Vitamin E is an effective antioxidant which prevents the activity of free radicals. This study was aimed to clarify the effect of vitamin E on the oxidative stress induced by chronic administration of BPA. Materials and methods: 30 female albino rats were divided into 3 groups (10/each); group1: control rats, group 2: rats treated with bisphenol A (20 mg/ kg.B.wt) for three months, and group 3: rats treated with bisphenol A (20 mg/kg.B.wt) for three months, then treated with BPA and vitamin E (0.57/100 g B.wt) for other 15 days. Results: BPA induced hormonal disrupt in liver and kidney dysfunctions and hyperlipidemia. Vitamin E ameliorated all these parameters. Conclusion: since we exposed to many harmful disruptions and oxidative stress compounds, we must take vitamin E as a protective agent.

Ameliorative effect of vitamin C against hepatotoxicity induced by emamectin benzoate in rats.

In the present study, we aimed to assess the potential protective effect of ascorbic acid (AA) against emamectin benzoate (EMB)-induced hepatotoxicity. For this purpose, biochemical, histopathological and analytical investigations were performed. Male Wistar rats were distributed into three groups, that is, a control group, an EMB group given 10 mg EMB/kg body weight (BW) by gavage and an EMB + AA group given 10 mg EMB/kg BW and vitamin C intraperitoneally (200 mg/kg). The duration of the treatment was 28 days and the duration of the study was 42 days. There was a statistically significant increase of all hepatic biomarkers, that is, aspartate aminotransferase, alanine aminotransferase and gamma-glutamyltransferase activities, and glycemia, in EMB-treated group when compared with the control group. Light microscopic observations revealed variable signs of hepatotoxicity in the EMB group, which were represented by alteration of normal hepatic architecture, inflammatory cell infiltration, hepatocellular steatosis and foci of necrosis at 28 and 42 days post-treatment. However, co-treatment with vitamin C reduced EMB-related liver toxicity and diminished the abnormal biochemical and architectural damage. Emamectin B1a and B1b residues were detectable in all plasma samples of treated rats at 14, 21 and 28 days of treatment. The drug liver tissue concentration was significantly lower in EMB + AA group compared with EMB group at 28 and 42 days. In conclusion, the findings of the present study clearly indicate a significant protective action of vitamin C against EMB hepatotoxicity.

Ameliorative Effect of Vitamin E on Azithromycin Induced Biochemical and Histological Changes in Liver Tissue of Rats

Ameliorative Effect of Vitamin E on Azithromycin Induced Biochemical and Histological Changes in Liver Tissue of Rats

Vitamin C alleviates surgical castration-induced dyslipidemia in male rats

Background and Aims: Androgen deprivation has been shown to be associated with dyslipidemia. Ameliorative effect of Vitamin C on dyslipidemia has also been reported. This study aimed at investigating the role of Vitamin C supplementation in castration-induced dyslipidemia. Materials and Methods: Twenty male rats were randomly divided in a blinded fashion into 4 groups (n = 5 each): Groups I and II were sham-castrated and received normal saline (1 ml/kg) and 1.25 g/kg Vitamin C, respectively, whereas Groups III and IV were rendered bilaterally castrated and received normal saline (1 ml/kg) and 1.25 g/kg Vitamin C for 4 weeks. Results and Conclusions: Castrated rats had reduced high-density lipoprotein, testosterone, estradiol, but increased low density lipoprotein, triglycerides, total cholesterol, and Castelli index and had no effect on follicle stimulating hormone when compared to sham-operated rats. Vitamin C supplements improved these parameters in normal and castrated rats. This study showed that castration-associated dyslipidemia and atherogenic risk in male rats is dependent on testosterone and estradiol. In addition, Vitamin C improves these parameters in normal and castrated rats by increasing testosterone and estradiol production, possibly from extra-testicular sites. However, there is a need for further study to ascertain the actual extra-testicular testosterone and estradiol production site.

Impact of the fungicide hexachlorobenzene on an in vitro model of intestinal barrier and the ameliorative effect of vitamin E

Impact of the fungicide hexachlorobenzene on an in vitro model of intestinal barrier and the ameliorative effect of vitamin E

Plasma and kidney distribution of emamectin benzoate in rats by ultra-performance liquid chromatography–tandem mass spectrometry, and protective effect of vitamin C

Aim Emamectin benzoate (Proclaim ® ) is a macrocyclic lactone semi-synthetic derivative of the avermectins. It is a mixture of at least 90% avermectin B1a benzoate (MAB1a) and at most 10% MAB1b salts [1] . The aim of this study is to investigate the plasma and kidney distribution of EMB in rats by ultra-performance liquid chromatography–tandem mass spectrometry (UPLC–MS/MS) and to evaluate the protective effects of vitamin C against toxicity of this biopesticide after a subacute toxicity study. Methods Male rats ( n = 21) were allocated into 3 groups of seven each: group I served as control rats; group II was given daily EMB at dose of 10 mg/kg b.w. by gavage; group III received EMB (10 mg/kg b.w.) and were co-administered with vitamin C intraperitoneally (200 mg/kg/day) during 28 days. Rats were followed-up for an additional 14 day-period to detect delayed occurrence or persistence of toxic effects. The residual concentrations of emamectin benzoate mixture B1a and B1b were determined in control, EMB, and EMB + VitC groups. Plasma and tissue homogenates were pretreated by protein precipitation with acetonitrile. In plasma samples at 14, 21, 28 and 42 days of experiment and in kidneys at 28 and 42 days of experiment, B1a and B1b concentrations were determined. Results A decrease in body weight, absolute and relative kidney weights in EMB-treated rats and a significant increase in EMB +VitC group, after 28 and 42 days of experiment, were observed. Emamectin B1a and B1b were found in all plasma samples of EMB and EMB + VitC rats in a time-dependent manner at 14 days [EMB group (B1a: 531.95 ± 98.31; B1b: 20.25 ± 10.71) and EMB + VitC (B1a: 436.70 ± 200.39; B1b: 15.12 ± 2.97)], 21 days [EMB group (B1a: 566.29 ± 103.91; B1b: 19.73 ± 3.00) and EMB + VitC group (B1a: 315.97 ± 73.72; B1b: 16.02 ± 4.00)] and 28 days of treatment [EMB group (B1a: 626.35 ± 159.32; B1b: 23.03 ± 8.19) and EMB + VitC group (B1a: 368.50 ± 152.22; B1b: 14.88 ± 7.28)]. However, those concentrations were higher in the EMB-treated group when compared with the EMB + VitC group. Moreover, at 42 days, there was no more residue detectable in the plasma of all treated rats. In EMB-treated rats, the drug kidney concentrations were significantly lower in EMB + VitC compared with EMB-treated rats at 28 days [EMB group (B1a: 24.98 ± 1.85; B1b: 3.63 ± 0.34) and EMB + VitC (B1a: 14.14 ± 1.24; B1b: 1.26 ± 0.29)] and 42 days post-treatment [EMB group (B1a: 0.87 ± 0.30; B1b: 0.04 ± 0.01) and EMB + VitC (B1a: 0.31 ± 0.15; B1b: 0.01 ± 0.00)]. Elevated concentrations of residues in plasma and kidneys of EMB-treated rats compared to those in EMB + Vit C-treated rats suggest an ameliorative effect of vitamin C. Conclusion EMB was widely distributed in rat plasma and kidneys and its concentrations in kidney increased in a time-dependent manner. Vitamin C, when administered at moderate doses and maintained for a long period, could reduce the accumulation of EMB in plasma and kidneys.

Newcastle disease virus (NDV) induces protein oxidation and nitration in brain and liver of chicken: Ameliorative effect of vitamin E

The present study was aimed at investigating the therapeutic efficacy of vitamin E on oxidative injury in brain and liver of Newcastle disease virus (NDV) challenged chickens. We have analyzed the xanthine oxidase (XOD) activity; uric acid (UA) levels and superoxide radical generation by using electron spin resonance spectroscopy. Further, protein oxidation, nitration and apoptosis were evaluated in the brain and liver of the control, NDV-infected and NDV+Vit. E treated groups. A significant elevation was observed in XOD activity and UA levels in brain (p<0.001) and liver (p<0.05) of NDV infected birds when compared to controls. Further, significant increase in the production of superoxides, enhanced intracellular protein carbonyls and nitrates were observed in the brain and liver of NDV-infected birds over healthy subjects. Apoptosis studies also suggested that a larger number of TUNEL positive cells were observed in brain and a moderately in liver of NDV-infected chickens. However, all these perturbations were significantly ameliorated in NDV+Vit. E treated chickens as compared to NDV-infected birds. Taken together, our results suggested that NDV-induced neuronal and hepatic damage at least in part mediates oxidative stress and on the other hand, supplementation of vitamin E mitigates NDV-induced oxidative damage thereby protects brain and liver of chickens. These findings could provide new insights into the understanding of NDV pathogenesis and therapeutic effects of dietary antioxidants.

Pathology of fenvalerate toxicity in broiler chicks and its amelioration with vitamin E

The present study was conducted to evaluate the histopathological alterations in experimentally induced fenvalerate toxicity and ameliorating effect of vitamin E in broiler chicks. For this study, one hundred fifty apparently healthy unsexed broiler chicks (White Leghorn) were randomly divided into five groups. The control chicks were fed with normal feed without fenvalerate. Group I and II were fed with 20 ppm/kg feed and 40 ppm/kg feed Fenvalerate respectively. Group III and IV chicks were fed with 20 ppm/kg feed and 40 ppm/kg feed Fenvalerate respectively along with Vitamin E @ 2.5 ml each (62.5 mg) in water. Grossly kidney showed enlargement, moderate to severe congestion with mild haemorrhages. Liver revealed paleness, congestion with areas of blotchy haemorrhages. Hydropericardium is noticed in heart. Thymus and spleen showed mild atrophy with petechial haemorrhages. Microscopically, kidney revealed mild fatty change, intertubular fibrous tissue proliferation and focal atrophy of renal tubules. Tubular necrosis in kidneys was evident in group II and IV. Periportal fibrosis, hyperplasia of bile ductular epithelium and individualization of hepatocytes were noticed in liver. Mild haemorrhages and mild to moderate depletion of lymphocytes were noticed in thymus, bursa and spleen. The ameliorative effect of vitamin E @ 2.5ml (62.5mg.vitamin E) was negligible. Toxic changes were noticed mainly in kidney followed by liver indicating the nephrohepato toxic nature of the fenvalerate. The changes in bursa and thymus are indicating the immunosuppressive effect.

Protective role of Vitamin E: on diazinon-induced hepatotoxicity by biochemical and histological alterations in Wistar rats

Background: Pesticides are developed for welfare of human beings, though they impose and challenge our existence by their long-term toxicity. Organophosphates such as diazinon contain phosphorus and derivatives of phosphoric acids. Aims and Objectives: To evaluate the toxic effects of diazinon in separate lower doses on hepatotoxicity and possible ameliorative properties of vitamin E on diazinon-induced alterations on biochemical and histological parameters on liver functions. Materials and Methods: Toxic effects of diazinon, dose levels 0 mg, 6 mg, 7.5 mg, and 10 mg/kg body weight daily orally for 30 days and ameliorative effect of vitamin E (2 mg) on diazinon-induced biochemical and histological alterations were investigated in Wistar albino male rats. The serum was used to evaluate the level of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), alkaline phosphatase (ALP), cholesterol, triglyceride, total protein, albumin, and malondialdehyde (MDA). Liver paraffin sections were cut into 5 µm thickness and stained with hematoxylin and eosin for light microscopic examination. Results: Diazinon resulted in an increase in MDA level significantly, decrease in albumin, total protein, cholesterol levels, and rise in AST and ALT levels. LDH and ALP levels were elevated significantly (p < 0.001). Hepatocytes showed pyknotic changes in nucleus, ballooning degeneration (fatty changes), periportal inflammation and Kupffer cells hyperplasia in diazinon-treated groups. Pretreatment of the rats with vitamin E showed an insignificant protection in diazinon-induced liver damage. Conclusion: In conclusion, this study suggests that diazinon induces hepatotoxicity in low doses and vitamin E partly ameliorates biochemical and histological alterations induced by diazinon.

Ameliorative Effect of Vitamin C on the Altered Tissue Ascorbate Levels in Wistar Rats Exposed to Chlorpyrifos and Lead Acetate for 98 Days

The present study was designed to evaluate the effects of chlorpyrifos, lead acetate, vitamin C alone and in combination on tissue ascorbate levels in Wistar rats. Rats of 150–200 g body weight were divided into eight groups of six animals each and were subjected to various daily oral treatment regimens for 98 days. Group C served as control receiving only corn oil, group CP received chlorpyrifos at 5.5 mg/kg in corn oil, group L received lead acetate at 100 ppm in water, whereas animals in group CP + L received a combination of chlorpyrifos at 5.5 mg/kg in corn oil and lead acetate at 100 ppm in water. Group VC received vitamin C at 100 mg/kg in water, group CP + VC received a combination of chlorpyrifos at 5.5 mg/kg and vitamin C at 100 mg/kg, group L + VC received lead acetate at 100 ppm in water and vitamin C at 100 mg/kg and group CP + L + VC received chlorpyrifos at 5.5 mg/kg, lead acetate at 100 ppm in water and vitamin C at 100 mg/kg. After 98-day exposure of chlorpyrifos and lead acetate, the concentration of ascorbate in liver, kidney and lung homogenates was decreased significantly as compared to the control group, besides a significant decrease was also observed in the homogenates of brain and heart tissues of chlorpyrifos and lead treatment groups, respectively. In groups receiving both chlorpyrifos and lead acetate, the concentration of ascorbate was significantly decreased in kidney, lung and liver homogenates. The study demonstrated that treatment of chlorpyriphos and lead treated rats with vitamin C significantly altered some of the important haematological parameters revealing the protective effect of this vitamin against haematological alterations induced by chlorpyriphos and lead.

Centratherum anthelminticum minimizes the risk of insulin resistance in fructose-induced type 2 diabetes

Ameliorative Effects of Vitamin C and E on Serum Lipid Profiles and Liver Enzymes on Fructose induced hyperglycaemia in Wistar RatsTanko Y.,Eze E. D.,Daja H. S., Jimoh A.,Mohammed K. A. and K.Y. Musa

Ameliorative effect of vitamin-C on lead-induced biochemical alterations in the serum of broilers

The present study was aimed to elucidate the ameliorative effect of vitamin C on biochemical alterations in broilers treated with lead acetate. One hundred and eight (1 day old) broiler chicks were reared for 2 weeks and randomly divided into 6 equal groups. Group I birds served as control. Group II and III birds were given lead acetate @ 250 and 500 ppm, respectively, while group IV and V were supplemented with vitamin C @ 40 mg L−1 water in addition to lead acetate @ 250 and 500 ppm, respectively. Group VI birds were supplemented with vitamin C @ 40 mgL−1 water in their normal feed. Total serum protein analysis revealed a significant decrease in lead treated birds while as AST, ALT, blood urea nitrogen (BUN), creatnine and uric acid revealed a significant increase but the values were modulated in vitamin C supplemented birds.

Ameliorative effect of vitamin E to mouse dams and their pups following exposure of mothers to chlorpyrifos during gestation and lactation periods

Pesticides are omnipresent in environment, water, fruits, and vegetables and are considered as risk factors for human health. Consumers are mainly exposed to pesticides through diet, and the main question to be answered concerns the impact of such exposure on health. In this study, we developed a mouse model to mimic consumer exposure. During gestation and lactation periods, the experimental mouse dams (M) received one of the following treatments: (a) diet-free of pesticides; (b) diet enriched with chlorpyrifos (CPF; 44.0 μg kg(-1)); c) diet + oral vitamin E (vit. E; α-tocopherol; 200 mg/kg/mouse); and (d) diet enriched with CPF (44.0 μg/kg + oral vit. E (200 mg/kg/mouse). At weaning, pups (P) and dams were killed, and organs as well as blood samples were collected. Compared with control results, CPF induced alteration of measured parameters (e.g. organ weight, alkaline phosphatase, urea, malondialdehyde, superoxide dismutase, and cholinesterase) either in mouse dams or in their offspring. Also, CPF induced histological impairment in kidney, liver, and ovary. Administration of vit. E in conjunction with CPF clearly alleviated deviation of these parameters than those of control ones. In conclusion, a dietary exposure of mice during gestation and lactation to low dose of CPF led to significant changes in the mother but also in the weaned animals that have not been directly exposed to this pesticide. These biological and histological modifications could be reversed by an oral supplementation of vit. E.

Ameliorative effect of vitamin C against 5-fuorouracil-induced hepatotoxicity in mice: A light and electron microscope study

5-Fluorouracil is one of the most widely used chemotherapeutic agents in case of hepatic neoplasms. The object of this study was to determine the effectiveness of vitamin C in alleviating 5-fluorouracil-induced hepatotoxicity in male mice. Thirty male albino mice were divided equally into 3 groups, each of 10 animals; group 1, mice received normal saline solution (control group); group 2, mice received 5-fluorouracil 80mg/kgb.wt./day intraperitoneally for 4weeks (5-fluorouracil group); group 3, mice received 5-fluorouracil 80mg/kgb.wt./day for 4weeks with daily injection of vitamin C (12mg/kgb.wt./day) for 4weeks. Animals of all groups were sacrificed and tissue samples from the liver were taken and processed for both light and electron microscopical examination. Light microscopic observations revealed that administration of 5-fluorouracil causes variable signs of hepatotoxicity which are represented by focal areas of liver cell necrosis with distortion of normal hepatic architecture; the hepatocytes showed vacuolated cytoplasm and pyknotic nuclei together with inflammatory cell infiltration. Dilated, congested hepatic sinusoids with active kupffer cells were also seen. Ultrastructure examination confirmed the light microscopic findings and demonstrated vacuolated hepatocytes cytoplasm, dilated endoplasmic reticulum, increased lysosomes, electron-dense mitochondria and pyknotic nuclei. Treatment with vitamin C with 5-fluorouracil attenuated 5-fluorouracil-induced hepatotoxicity and reverted the abnormal structural changes to near normal. In conclusion, these results suggest that vitamin C has a protective potential in ameliorating 5-fluorouracil-induced hepatotoxicity.

Which exposure stage (gestation or lactation) is more vulnerable to atrazine toxicity? Studies on mouse dams and their pups

Either during gestation or lactation, the experimental mouse dams received one of the following treatments: (a) diet free of pesticide; (b) diet enriched with atrazine (ATZ); 31.0 μg kg−1; (c) diet free of pesticide + oral vitamin E (α-tocopherol; 200 mg kg−1 per mouse); and (d) diet enriched with ATZ (31.0 μg kg−1) + oral vitamin E (200 mg kg−1 per mouse). At the weaning, pups and dams were killed and selected organs and blood samples were collected for analyses. Compared with the control results, ATZ induced alteration in a number of biochemical and histopathological parameters either in the dams or their offspring. The ameliorative effect of vitamin E, based on estimating the “Ameliorative Index; AI” to malondialdehyde (MDA) and superoxide dismutase (SOD) ranged between 0.95 and 1.06 (≈1.0) for the dams and the pups either in gestational or lactational exposure routes. In general, the mouse pups were more vulnerable to ATZ toxicity than their mothers and exposure during gestation was suggested to be more effective than during lactation. The findings may support the need to further investigating the adverse effects of exposure to low doses of commonly used pesticides, especially during pregnancy and breast-feeding as well as effects on newborn child.

Carbofuran Induced Oxidative Stress in Rat Heart: Ameliorative Effect of Vitamin C

The aim of this study was to evaluate the effect of carbofuran on the levels of certain biomarkers in heart of rat exposed to sublethal concentrations of pesticide for 30 days after each interval of 24 h. The ameliorative effect of vitamin C by pretreatment of rats was also monitored. The results indicated that the activities of acetylcholinesterase and lactate dehydrogenase (LDH) decreased significantly in rat heart tissues, the extent of inhibition being concentration dependent. In contrast, the level of LDH increased in serum. The levels of malondialdehyde, total thiols, and glutathione were significantly elevated whereas the activities of antioxidant enzymes such as superoxide dismutase, catalase, and glutathione-S-transferase were remarkably decreased in rat heart tissues. The serum concentrations of cholesterol increased by 47 and 77% and high density lipids decreased by 35 and 64%, respectively, due to exposure to 5 and 10% LD50of carbofuran. The prior treatment of rats with vitamin C (100 mg kg−1body weight) exerted significant ameliorative effect. The recovery was higher at low carbofuran concentration (5%) tested. The results indicated that carbofuran induced oxidative stress and caused damage to cardiac tissues, which could be recovered by prior application of vitamin C.

Ameliorative effect of vitamin E on potassium dichromate-induced hepatotoxicity in rats

Hexavalent chromium [Cr (VI)]-mediated oxidative stress causes severe hepatic toxicity. This study aims to investigate the protective role of oral vitamin E administration against potassium dichromate (K2Cr2O7)-induced hepatotoxicity. Adult male rats (Rattus norvegicus, n=24) weighing 150–180g were used and divided into 4 groups (n=6 per group): the control group received distilled water; control+vitamin E group received vitamin E (100mg/kg b.w.); Cr group received K2Cr2O7 (8mg/kg b.w.), and Cr+vitamin E group received K2Cr2O7+vitamin E. All treatments were administered orally on a daily basis for 6weeks.There was a significant accumulation of Cr in the livers of the Cr group compared with the control group. In addition, exposure to K2Cr2O7 induced significant increases in the level of thiobarbituric-reactive substances (TBARS) and significant decreases in glutathione (GSH) content and superoxide dismutase (SOD) activity in the Cr group compared with the control group. Moreover, livers of the Cr group showed major histological alterations, such as severe necrosis, increased lymphocytic infiltration, and a significant decrease in the DNA content. Oral vitamin E administration concomitant with K2Cr2O7 ameliorated all these changes and resulted in normal hepatic histological and cellular contents. In conclusion, oral vitamin E administration has a hepatoprotective role against K2Cr2O7-induced hepatotoxicity in rats.

Effects of indirect exposure of mice pups to endosulfan via their dams during gestation and lactation periods and the ameliorative effect of vitamin E

During gestation and lactation, the experimental mice dams received one of the following treatments: (a) diet free of pesticide; (b) diet enriched with endosulfan (END); 30.0 µg kg(-1); (c) diet free of pesticide + oral vitamin E (α-tocopherol; 200 mg kg(-1) per mouse); and (d) diet enriched with END (30.0 µg kg(-1)) + oral vitamin E (200 mg kg(-1) per mouse). At weaning, pups and dams were killed, and selected organs as well as blood samples were collected for analyses. Compared with the control results, END induced alteration in a number of biochemical and histopathological parameters either in the dams or their offspring. The ameliorative effect of vitamin E to superoxide dismutase based on the "ameliorative index (AI)" for mothers and pups was 0.84 and 0.72, respectively. The AI for malondialdehyde reached a maximum value of nearly equal to 1.0 for dams or pups. For butyryl cholinesterase, the AI was 0.90 and 0.94 for dams and pups, respectively. In conclusion, a dietary exposure during gestation and lactation to low dose of END caused significant changes in the mother but also in the weaned animals that had not been directly exposed to this pesticide. These biological and histological alterations could be reversed to a great extent by oral supplementation of vitamin E.

Experimental Studies on the Effect of Chlorpyriphos and Lead Acetate on Biochemical Parameters in Wistar Rats with Special Reference to Ameliorative Effect of Vitamin C

The present study was designed to evaluate the effects of chlorpyriphos, lead acetate, vitamin c alone, and in combination on various biochemical parameters in wistar rats. Rats of 150–200 g body weight were divided into eight groups of six animals each and were subjected to various daily oral treatment regimes for 98 days. Group I served as control receiving only corn oil, group II received chlorpyriphos at 5.5 mg/kg in corn oil, group III received lead acetate at 100 ppm in water, whereas animals in group IVth received a combination of chlorpyriphos at 5.5 mg/kg in corn oil and lead acetate at 100 ppm in water. Group Vth received vitamin C at 100 mg/kg in water, group VIth received a combination of chlorpyriphos at 5.5 mg/kg and vitamin C at 100 mg/kg, group VIIth received lead acetate at 100 ppm in water and vitamin C at 100 mg/kg and group VIIIth received chlorpyriphos at 5.5 mg/kg, lead acetate at 100 ppm in water and vitamin C at 100 mg/kg. Chlorpyriphos and lead acetate alone or in combination elevated the activities of plasma aminotransferases, phosphatases, creatinine and blood urea nitrogen where as decreased the total plasma protein levels both due to chlorpyriphos and lead acetate treatment alone or in combination. The results showed that alterations in the biochemical parameters induced by co-exposure to chlorpyriphos and lead were mitigated by pretreatment with vitamin C. It is recommended that further research be geared towards identifying more agents that may ameliorate such adverse effects.