Long-term exposure to bisphenol-A causes oxidative stress-related alterations at the genetic and cellular levels in the mature ovary of adult zebrafish.

Abstract

Bisphenol-A (BPA) is categorized as a major endocrine-disrupting chemical (EDC) used to manufacture many plastic products. BPA affects reproductive performance and promotes infertility by causing hormonal imbalance, mitochondrial dysfunction, and altered gene expression. The present investigation aimed to evaluate the effects of BPA exposure for 28days on the activity or level of antioxidant response elements (AREs), mRNA expressions of antioxidant genes, and histomorphological changes in the ovary of adult zebrafish. The adult female zebrafish were randomly divided into four experimental groups, viz. control, vehicle (0.01% ethanol), low dose (BPA: 350µg/L), and high dose (BPA: 700µg/L) exposure groups. After BPA exposure in both groups, superoxide dismutase (SOD) activity and total antioxidant capacity (TAC) level were significantly (p<0.05) decreased in the zebrafish ovary. Whereas, catalase (CAT) activity and malondialdehyde (MDA) level were significantly (p<0.05) increased in both treatment groups. The sod mRNA expression was significantly (p<0.05) down-regulated in the high-dose BPA-exposed group. Whereas, cat and nuclear factor erythroid 2-related factor 2 (nrf2) mRNA expressions were significantly (p<0.05) up-regulated in both BPA-treated groups. Noticeable histomorphological alterations were recorded in the ovary of zebrafish exposed to low and high doses of BPA. The alterations in the activity of ARE, mRNA expressions of antioxidant genes, and histopathological changes suggest that exposure to BPA can cause endocrine disruption and damage to the ovary of adult zebrafish caused by oxidative stress.