Prospective role of ascorbic acid (vitamin C) in attenuating hexavalent chromium-induced functional and cellular damage in rat thyroid.

Occupational exposure to toxic heavy metals may render industrial workers with thyroid-related problems. Here, we examined the role of ascorbic acid (vitamin C) against hexavalent chromium Cr (VI)-induced damage in rat thyroid gland. Potassium dichromate (K2Cr2O7) and ascorbic acid doses were 60 microg and 120 mg kg(-1) body wt (intraperitoneally [i.p.]) respectively. Treatment regimens were group I rats, saline treated control; group II, only K2Cr2O7; group III, ascorbic acid 1 hour prior K2Cr2O7; group IV, simultaneous doses of ascorbic acid and K2Cr2O7, and group V, a combined premix dose of ascorbic acid and K2 Cr2O7 (2:1 ratio). Blood samples were taken before dosing the animals and 48 hours post exposure to determine the serum thyroid-stimulating hormone (TSH), free triiodothyronine (FT3) and free thyroxine (FT4) concentrations. Toward end of experiment, rats were sacrificed and thyroid glands were processed to evaluate the extent of cellular insult. Results showed significantly increased TSH and decreased FT3 and FT4 concentrations in groups II, III and IV rats as compared to control levels (p < 0.05). In contrast, in group V rats, serum TSH, FT3 and FT4 concentrations neared control concentrations. Histopathologically, protective effect of ascorbic acid was found in group V rats only, where thyroid gland structure neared control thyroid except the follicular size that was decreased (p < 0.05). Follicular density was no different from control. Basal laminae were intact, interfollicular spaces were normal. Colloid retraction and/or reabsorption were reduced maximally. Epithelial cell height was no different from control; epithelial follicular index increased only 1.3 fold, whereas nuclear-cytoplasmic (N/C) ratio was decreased by 14% only. The study indicates that the ascorbic acid may have the potential to protect thyroid gland from chromium toxicity; however, the study warrants further in-depth experimentation to precisely elucidate this role.

Aqueous extract of Phyllanthus amarus inhibits chromium(VI)-induced toxicity in MDA-MB-435S cells.

Cr(VI) (hexavalent) is a very strong oxidant which causes high cytotoxicity through oxidative stress in tissue systems. Its abundance in groundwater and drinking water in several parts of the world has been noted to cause severe toxicity to both flora and fauna. This study evaluated the effects of aqueous extract of Phyllanthus amarus Schum. & Thon. against Cr(VI)-induced oxidative toxicity in vitro in MDA-MB-435S human breast carcinoma cells, along with an estimation of its antioxidant potential, inhibition of lipid peroxidation and determination of its polyphenolic composition. The extract showed significant (P<0.05) potential in scavenging free radicals (DPPH() and ABTS()(+)) and Fe(+3), and in inhibiting lipid peroxidation. A distinct decline in Cr(VI)-induced cytotoxicity was noticed in MDA-MB-435S cells with an increase in extract dosage. Furthermore, the extract proved to contain a high content of phenolic compounds which were found to have strong and significant (P<0.05) positive correlations to free-radical scavenging potential, lipid peroxidation inhibition capacity and cyto-protective efficiency against Cr(VI)-induced oxidative cellular damage. HPLC analysis identified some of the major phenolic compounds in it. It was concluded that P. amarus aqueous extract has high antioxidant potential (by virtue of its phenolic constituents) which simultaneously inhibits Cr(VI)-induced oxidative toxicity to MDA-MB-435S cells.

Protective role of vitamin E on nickel and/or chromium induced oxidative stress in the mouse ovary.

In the present study, we report the invivo effects of nickel chloride (NiCl2; 8 and 16 mg/kg body weight) and/or potassium dichromate (K2Cr2O7; 5 and 10mg/kg body weight) in the ovary of adult mice. The protective role of vitamin E (2mg/kg body weight) along with their combination was also studied. Nickel and/or chromium to mice enhanced the levels of lipid peroxides in the ovary, which was accompanied by a significant decline in the levels of protein, glutathione, total ascorbic acid and activities of superoxide dismutase and catalase. Supplementation of vitamin E along with NiCl2 + K2Cr2O7 significantly lowered the levels of lipid peroxidation and enhanced the antioxidant status. Findings of the present study suggest that vitamin E exerts its protective effect against nickel and/or chromium induced toxicity by preventing lipid peroxidation and protecting antioxidant system in the mouse ovary.