Novel Insights into Cadmium-Induced Liver Toxicity in Largemouth Bass (Micropterus salmoides): Oxidative Stress, Inflammatory Response, and Mitochondria-Mediated Apoptosis Pathway.

In this study, 360 healthy juvenile largemouth bass, averaging body weights of 11.26 ± 0.49 g, were randomly assigned to four experimental groups. These groups were exposed to water environments containing different concentrations of cadmium (Cd): 0 mg/L for the control (Con) group, 0.9804 mg/L for the low-cadmium (LCd) group, 1.9608 mg/L for the medium-cadmium (MCd) group, and 9.804 mg/L for the high-cadmium (HCd) group, over a duration of 21 days, to study how different levels of Cd impact the liver. Ultrastructural changes manifest as nuclear deformation, blurred cell membrane boundaries, mitochondrial swelling, matrix dissolution, cristae rupture, and disappearance. TUNEL analysis indicates that the apoptotic rate of hepatocytes increases with increasing Cd concentration. Compared with the Con group, serum biochemical results showed that the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), glucose (GLU), and urea (UREA) were significantly elevated in the HCd group. With increasing Cd concentration, the activities of hepatic catalase (CAT), superoxide dismutase (SOD), and glutathione (GSH) were significantly altered, accompanied by a reduction in ATP content and an increase in the malondialdehyde (MDA) levels. Analysis of inflammatory gene expression showed upregulation of pro-inflammatory genes (IL-1β, TNF-α, and IL-6) and downregulation of the anti-inflammatory gene IL-10. In addition, significant changes in the mRNA levels of apoptosis-related genes were observed in these Cd-exposed groups. Collectively, these findings consistently indicate that Cd exposure can lead to liver injury in largemouth bass by inducing oxidative stress, inflammatory responses, and apoptosis.