Saeed Yendigeri

Environmental arsenic contamination and its health effects in a historic gold mining area of the Mangalur greenstone belt of Northeastern Karnataka, India.

This report summarizes recent findings of environmental arsenic (As) contamination and the consequent health effects in a community located near historic gold mining activities in the Mangalur greenstone belt of Karnataka, India. Arsenic contents in water, hair, nail, soil and food were measured by FI-HG-AAS. Elemental analyses of soils were determined by ICP-MS (inductively coupled plasma-mass spectrometry). Of 59 tube-well water samples, 79% had As above 10 μg L(-1) (maximum 303 μg L(-1)). Of 12 topsoil samples, six were found to contain As greater than 2000 mg kg(-1) possibly indicating the impact of mine tailings on the area. All hair and nail samples collected from 171 residents contained elevated As. Arsenical skin lesions were observed among 58.6% of a total 181 screened individuals. Histopathological analysis of puncture biopsies of suspected arsenical dermatological symptoms confirmed the diagnosis in three out of four patients. Based on the time-course of As-like symptoms reported by the community as well as the presence of overt arsenicosis, it is hypothesized that the primary route of exposure in the study area was via contaminated groundwater; however, the identified high As content in residential soil could also be a significant source of As exposure via ingestion. Additional studies are required to determine the extent as well as the relative contribution of geologic and anthropogenic factors in environmental As contamination in the region. This study report is to our knowledge one of the first to describe overt arsenicosis in this region of Karnataka, India as well as more broadly an area with underlying greenstone geology and historic mining activity.

α-Tocopherol ameliorates nickel induced testicular oxidative and nitrosative stress in albino rats.

Abstract Background: Heavy metals generate free radicals and induce oxidative and nitrosative stress with depletion of antioxidants. In this study, we have evaluated the beneficial effects of α-tocopherol against nickel sulfate exposed testicular dysfunction. Methods:We studied the effect of supplementation of α-tocopherol (10 mg/100 g body weight, i.m.) on nickel sulfate (2.0 mg/100 g body weight, i.p.) induced testicular oxidative and nitrosative stress in Wister strain male albino rats. Serum and testicular nitric oxide, L-ascorbic acid and serum α-tocopherol concentrations were evaluated. We also evaluated sperm count, motility and histopathology of testes. Results:Nickel treated rats showed significantly decreased body weight, testicular somatic index, sperm count, sperm motility, serum and testicular L-ascorbic acid concentration and serum α-tocopherol level as compared to their controls. However, simultaneous treatment with nickel sulfate and α-tocopherol produced a remarkable improvement of all the above parameters when compared with treatment with nickel alone. Nickel treated rats also had significantly increased serum and testicular nitric oxide concentrations as compared to their controls. However, simultaneous treatment with nickel sulfate and α-tocopherol significantly decreased nitric oxide concentrations in both serum and testes, respectively, as compared to nickel treatment alone. Histopathology of the testes revealed tortuous seminiferous tubules, loss of spermatogenesis process (>75%), congestion and necrosis in nickel sulfate treated rats, whereas rats simultaneously treated with nickel sulfate and α-tocopherol had almost normal seminiferous tubules and near normal spermatogenesis as compared to nickel alone treated rats. Conclusions: Nickel sulfate treatment causes testicular oxidative and nitrosative stress in albino rats, but simultaneous supplementation of α-tocopherol was found to be beneficial in combating against such stresses.

α-tocopherol supplementation prevents lead acetate and hypoxia-induced hepatic dysfunction

Objective: Lead (Pb) is a long-known poison of environment and industrial origin. Its prolonged exposure affects cellular material and alters cellular genetics and produces oxidative damages. In this study, we investigated the exposure of chronic sustained hypoxia or lead acetate alone or in combination with or without supplementation of α-tocopherol on hepatic oxidative and nitrosative stress in rats. Materials and Methods: The rats weighing 165 ± 5 g were exposed to chronic sustained hypoxia (10% oxygen) or lead acetate (25 mg/kg of body weight, intraperitoneally) alone or in combination with or without supplementation of α-tocopherol (10 mg/100 g b.wt, intramuscularly). The body weight of all the rats was recorded on the day 1 of the treatment and the day of sacrifice. Serum lipid profile was estimated by using a biochemical analyzer. Oxidant and enzymatic antioxidants status was evaluated by using spectrophotometer. Serum levels of hypoxia inducible factor-1 alpha (HIF-1α) and vascular endothelial growth factor (VEGF) were measured by using ELISA technique. Histopathological assessments of hepatic tissue were also done. Results: Exposure of both lead and hypoxia showed decreased body weight, altered serum lipid profile, oxidant and enzymatic antioxidants status, serum HIF-1α and VEGF concentrations. Simultaneous α-tocopherol supplementation showed beneficial effects to all these alterations. Histopathological observations also showed hepatic degenerative changes after lead or hypoxia exposure either alone or in combination, but remarkable improvement has been noticed after α-tocopherol supplementation. Conclusion: Supplementation of α-tocopherol is beneficial to counter both lead acetate and hypoxia induced hepatic cytotoxicities possibly by reducing oxidative and nitrosative stress.

Protective effect of Vitamin E (a-tocopherol) on nickel-induced alteration of testicular pathophysiology in alloxan-treated diabetic rats

Background and Aim: Diabetes mellitus is a global problem associated with increased formation of free radicals and decrease in antioxidant potential. Nickel generates free radicals and induces oxidative and nitrosative stress with depletion of antioxidants. Vitamin E is the most effective chain-breaking antioxidant against lipid peroxidation. Therefore, the present study was intended to evaluate the possible protective effect of Vitamin E (α-tocopherol) on oxidative stress in the testis of diabetic rats exposed to nickel. Methods: Diabetes was induced by alloxan monohydrate (15 mg/100 g b.wt, i.p.) in adult male Wistar albino rats. Diabetic rats in respective groups were exposed to nickel sulfate (2.0 mg/100 g b.wt, i.p) and α-tocopherol (10 mg/100 g b.wt, i.m.) alone as well as in combination on alternate days until the tenth doses. Testicular cholesterol and protein, aspartate aminotransferase (AST), alanine aminotransferase (ALT), nitric oxide, and lipid peroxide were evaluated by ultraviolet-visible spectrophotometer. Testicular histopathology was also evaluated. Results: Exposure of diabetes and nickel showed significantly decreased body weight, testicular-somatic index, testicular cholesterol and protein, AST, ALT, nitric oxide, and lipid peroxide levels. Simultaneous α-tocopherol supplementation showed remarkable improvement in all these alterations. We observed damage in testicular architecture with, tortuous seminiferous tubules, foci of congestion, necrosis, loss of spermatogenesis > 75% and loss of germ cell layer in diabetic and nickel-exposed diabetic rats. Testis of simultaneous α-tocopherol supplemented diabetic rats showed many normal seminiferous tubules and normal spermatogenesis (≥50%). Conclusion: Vitamin E (α-tocopherol) supplementation could exert a protective effect on the testis of diabetic rats exposed to nickel by suppressing the increased oxidative stress.

Sub-chronic indomethacin treatment and its effect on the male reproductive system of albino rats: possible protective role of black tea extract

Abstract Background: Indomethacin is commonly used as a nonsteroidal anti-inflammatory drug (NSAID) to treat inflammation, arthritis and joint pains. Unfortunately, it has a wide range of adverse effects on the physiological system, including gonads. This study aimed to assess possible beneficial effects of black tea extract (BTE) against indomethacin-induced alteration of gonadal hormone levels in male rats. Methods: Adult male rats were divided into Group I (control), Group II (indomethacin, 5 mg/kg body weight [bwt.]; i.p., 21 days), Group III (BTE, 2.5 g tea leaf/dL of water, i.e. 2.5% of aqueous BTE, orally, 21 days) and Group IV (indomethacin+BTE, 21 days). Sperm count and motility, serum luteinising hormone (LH), follicle-stimulating hormone (FSH) and testosterone, along with histopathology of testes were studied. One-way ANOVA, followed by post-hoc t-test were conducted. Results: Indomethacin-treated rats showed significant decrease in testicular weight, sperm count, sperm motility, serum gonadotropins and testosterone concentrations. Histopathology of the testes showed tortuous and distorted seminiferous tubules, marked thickening of the tubular basement membrane, reduced spermatogenesis process (>30%) and marked decrease in the number of interstitial cells of Leydig in indomethacin-treated rats. Interestingly, rats supplemented with BTE showed remarkable improvements in testicular weight gain, sperm count and motility, serum gonadotropins and testosterone concentrations, along with testicular histopathology. Conclusions: The results suggest that BTE might have potential ameliorative effects against sub-chronic indomethacin-induced alteration of gonadal hormone levels in male albino rats.