Hexavalent chromium (Cr6+) induces oxidative stress, inflammatory response, apoptosis, and DNA damage in the liver of largemouth bass by inhibiting the Nrf2-Keap1 signal pathway.

Heavy metal pollution poses a significant threat to the growth and health of fish, causing substantial economic losses in aquaculture. This study investigates the toxic effects of Cr⁶⁺ on the liver of Largemouth bass (Micropterus salmoides). Juvenile Largemouth bass were randomly divided into a control group (CON) and a chromium stress group (Cr⁶⁺), and subjected to a 96-h exposure test with Cr⁶⁺ at 96-h LC₅₀ concentration. The results showed that in the Cr⁶⁺ group, liver cell nuclei were condensed, cells exhibited vacuolation, liver sinusoidal spaces were enlarged, and cell contours were unclear. Compared to the CON group, the Cr⁶⁺ group had significantly reduced activities of liver superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT), with a significant decrease in T-AOC levels and a significant increase in MDA content (p < 0.05). Additionally, the relative mRNA expression levels of CAT, SOD, and GSH-Px were significantly decreased in the Cr⁶⁺ group (p < 0.05). The Nrf2-Keap1 Signal Pathway showed a significant increase in the relative mRNA expression of Nrf2 and a significant decrease in the relative mRNA expression of Keap1 in the Cr⁶⁺ group (p < 0.05). Furthermore, inflammatory response, apoptosis, and DNA damage were observed in the liver of Largemouth bass: the relative mRNA expression levels of interleukin-1β (IL-1β), interleukin-8 (IL-8), interleukin-15 (IL-15), and tumor necrosis factor-α (TNF-α) were significantly increased in the Cr6 + group (p < 0.05); the relative mRNA expression levels of Caspase-3, Caspase-8, Caspase-9, and Bax were significantly increased, while the Bcl-2 was significantly decreased; Tail length, Tail DNA (%), and Olive tail moment of liver cells were significantly increased (p < 0.05). In summary, Cr⁶⁺ induces oxidative stress, inflammatory response, apoptosis, and DNA damage in the liver of Largemouth bass by inhibiting the Nrf2-Keap1 signal pathway, thus affecting the health of the fish.