RETRACTED: Ameliorative effect of vitamin C on hexavalent chromium-induced delay in sexual maturation and oxidative stress in developing Wistar rat ovary and uterus

Abstract

Hexavalent chromium (CrVI) is a highly toxic metal and major environmental pollutant and is extensively used in more than 50 industries. The major route of CrVI exposure for the general population is oral intake. Chromium is considered an important nutrient responsible for carbohydrate metabolism. However, excess CrVI exposure is associated with various pathological conditions including reproductive dysfunction. CrVI can traverse the placental barrier and cause wide range of abnormalities in fetal development. Cr is transported to offspring through mother's milk in lactating women exposed to CrVI. Therefore, the present study was carried out to determine the toxic effects of lactational CrVI exposure on ovary and uterus and the beneficial role of vitamin C in preventing/ameliorating the toxic effects of CrVI in developing female Wistar rats. Generation of oxidative stress is considered one of the plausible mechanisms behind Cr-induced cellular deteriorations. The present study evidenced a decrease in the specific activities of antioxidants, serum testosterone and progesterone and an increase in the levels of H₂O₂, lipid peroxidation (LPO) and follicle stimulating hormone in rats exposed to CrVI when compared to control. CrVI exposure also delayed the sexual maturation and extended the estrous cycle. Simultaneous administration of vitamin C significantly prevented the increase in LPO and enhanced the antioxidant status. These results suggest the protective effect of vitamin C against the CrVI exposure-induced toxicity and attest the significance of antioxidants in diet.

Hexavalent Chromium-Induced Apoptosis in Rat Uterus: Involvement of Oxidative Stress

“…2 Exposure to Cr(VI) has been reported to cause a reproductive toxicity in human and laboratory animals. 5,6 These effects are produced by a direct action of Cr on reproductive organs. 7 Delayed sexual maturation and reduced fertility were observed in female mice offspring treated with Cr(III) and Cr(VI) compounds.…”

“…However, fewer studies have been conducted to evaluate the toxicity of Cr(VI) in female reproductive tract. 6 Therefore, the aim of this work is to investigate the effect of Cr(VI) subacute treatment on rat uterus and the implication of oxidative stress and apoptosis in this organ. To this end, the status of the oxidative stress was evaluated by biomarkers such superoxide anion production, lipid peroxidation (LPO), metallothionein (MT) levels, and catalase (CAT) activity.…”

“…This result was in accordance with that of Samuel et al 17 The decrease in superoxide dismutase (SOD) activity in animals exposed to a high dose of metals is associated with the increase of O ·− 2 , which has been shown to inhibit CAT. [6][7][8][9][10][11][12][13][14][15][16][17] Therefore, the decrease in CAT activity may explain the early elevated ROS levels, since it is a crucial enzyme involved in the detoxification of ROS. 17 Apoptosis is a genetically regulated cellular suicide mechanism in which multiple signaling pathways are implicated.…”

Effect of Simvastatin on Sodium Dichromate-Induced Lung Injury in Rats

“…The mechanism of lung toxicity of Cr(VI) compounds has not been clearly documented; however, chromates are readily taken up by cells and reduced to reactive Cr species, which may also result in the generation of reactive oxygen species (ROS) (14,15). Cr(VI) is rapidly converted to Cr(III) intracellularly, and can induce apoptosis through different mechanisms (14,15).…”

“…Cr(VI) is rapidly converted to Cr(III) intracellularly, and can induce apoptosis through different mechanisms (14,15).…”