Cadmium-Induced Oxidative Damage and the Expression and Function of Mitochondrial Thioredoxin in .

is a unique aquatic invertebrate native to China, whose habitat is highly susceptible to environmental pollution, making it an ideal model for studying aquatic toxicology. Mitochondrial thioredoxin (Trx2), a key component of the Trx system, plays an essential role in scavenging reactive oxygen species (ROS), regulating mitochondrial membrane potential, and preventing ROS-induced oxidative stress and apoptosis. This study investigated the toxicity of cadmium (Cd) on and the role of Trx2 (Trx2) in Cd detoxification. The results showed that Cd stress altered the activities of T-SOD and CAT, as well as the contents of GSH and MDA in the intestine. After 96 h of exposure, histological damages such as vacuolization, cell necrosis, and mitophagy were observed. Suggesting that Cd stress caused oxidative damage in Furthermore, with the prolongation of stress time, the expression level of intestinal Trx2 mRNA initially increased and then decreased. The recombinant Trx2 (rTrx2) protein displayed dose-dependent redox activity and antioxidant capacity and enhanced Cd tolerance of . After RNA interference (RNAi) with Trx2, significant changes in the expression of apoptosis-related genes (-3, , -2, and -) were observed. Proving that Trx2 rapidly responded to Cd stress and played a vital role in mitigating Cd-induced oxidative stress and apoptosis. Our study demonstrated that Trx2 is a key factor for to endure the toxicity of Cd, providing foundational data for further exploration of the molecular mechanisms underlying heavy metal resistance in .