Persistent hexavalent chromium exposure impaired the pubertal development and ovarian histoarchitecture in wistar rat offspring.

Hexavalent chromium (CrVI) is a highly toxic metal and a major environmental pollutant. Several studies indicate that CrVI exposure adversely affects reproductive function. We reported that maternal Cr exposure resulted in Cr accumulation in the reproductive organs of female offsprings. CrVI can cross the placental barrier and also can be passed through breastfeeding. The present investigation aimed to determine the persistent (in utero through puberal period) CrVI exposure-induced toxic effects on the reproductive functions of mother and the offspring. Induction of oxidative stress is one of the plausible mechanisms behind Cr-induced cellular deteriorations. Mother rats exposed to CrVI showed reduced reproductive outcome, while the offsprings showed higher accumulation of Cr in ovary, altered steroid, and peptide hormones. Specific activities of antioxidant enzymes were decreased and associated with increased levels of H2 O2 , and lipid peroxidation. CrVI exposure also damaged the ovarian histoarchitecture in various age groups studied. CrVI exposure also delayed the sexual maturation. Results from the present investigation suggest that CrVI exposure from in utero through puberal period significantly damaged the pubertal development through altered antioxidants, anemia, and altered hormone levels. These changes were associated with damaged ovarian histoarchitecture and extended estrous cycle in developing Wistar rats.

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

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.

Gestational cadmium exposure-induced ovotoxicity delays puberty through oxidative stress and impaired steroid hormone levels.

Cadmium (Cd), an environmental pollutant, has been shown to be highly toxic to both humans and animals. Its widespread industrial use has led to its accumulation in the environment. Cd has been shown to target multiple organs following acute intoxication, causing nephrotoxicity, immunotoxicity, osteotoxicity, and reproductive toxicity. Cd can cross the placental barrier and cause a wide range of defects during fetal development. The current study was aimed to assess the effect of Cd on the female reproductive system. Female rats were exposed to Cd [50/200 ppm] from embryonic day 9 to 21 through drinking water. Serum steroid hormone concentrations, hematological parameters, antioxidant enzyme levels, and ovarian histopathology were described. Water consumption, gravid uterine/body weight decreased in both the doses of Cd-treated dams. The hematological parameters analyzed in rat pups showed a significant reduction in both doses of Cd studied, while hemoglobin showed a significant reduction in 200 ppm Cd treatment alone. MCHC levels did not show any variation in 50 ppm Cd treatment, while 200 ppm Cd treatment significantly increased. Specific activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, and serum testosterone, estradiol, and progesterone were significantly decreased. The levels of hydrogen peroxide and lipid peroxidation were increased in 50 and 200 ppm Cd-treated rats. These changes were accompanied with disrupted ovarian histoarchitecture, an extended estrous cycle, and delayed pubertal onset in Cd-treated rats. The data generated from the present study suggest that gestational Cd treatment induces ovarian toxicity and reproductive dysfunction through increased oxidative stress.