Insights into the toxic impact of long-term exposure to diethyl phthalate on commercially important species Catla (Labeo catla)

Diethyl phthalate (DEP), used as a plasticizer, is more prevalent in the aquatic environment due to its widespread usage in plastics, cosmetics, and numerous pharmaceutical industries. It is a potential endocrine disruptor, but the underlying mechanism in fish needs to be investigated. The present study evaluated the toxic impacts of DEP exposure for 30 days on commercially important fish Labeo catla (Catla). Alterations at multiple level endpoints of the hypothalamic–pituitary–gonadal axis (HPG axis) were assessed. DEP-induced changes in oxidative stress, histopathological changes (liver, kidney and brain) and bioaccumulation in fish muscle were also evaluated. DEP exposure to 1/10th (1.62 mg/L) and 1/50th (0.32 mg/L) LC50 dose for 30 days to Catla revealed that it stimulated the expression of kisspeptin (Kiss 1 and Kiss 2) genes in the hypothalamus, leading to an increased GnRH concentration (36.75%) in the higher dose. The brain FSH levels increased by 11.24 and 55.42% times than control in both the doses. This led to an increase in circulating sex steroids E2 (41.62%) and 11 KT (24.59%) and eventually triggered hepatic Vtg production (23.90%) in a dose-dependent manner. DEP exposure lowered the concentration of antioxidants superoxide dismutase (SOD) and catalase (CAT), the effect being more pronounced in the higher dose. The histopathological alterations, such as hepatocyte vacuolization, sinusoidal congestion, loss of brush border, degeneration of lumen, infiltration of eosinophilic cells in liver, kidney and brain, respectively, were noted. This pioneering study could provide detailed insight into the endocrine disruptive potential of DEP in fish, as evidenced by its impact at multiple endpoints, even at low doses after 30 days of exposure. The output of this investigation thus emphasized the need for regular monitoring of DEP for ecological risk assessment.