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

<i>Phascolosoma esculenta</i> 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 <i>P. esculenta</i> and the role of <i>P. esculenta</i> Trx2 (<i>Pe</i>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 <i>P. esculenta.</i> Furthermore, with the prolongation of stress time, the expression level of intestinal <i>Pe</i>Trx2 mRNA initially increased and then decreased. The recombinant <i>Pe</i>Trx2 (r<i>Pe</i>Trx2) protein displayed dose-dependent redox activity and antioxidant capacity and enhanced Cd tolerance of <i>Escherichia coli</i>. After RNA interference (RNAi) with <i>Pe</i>Trx2, significant changes in the expression of apoptosis-related genes (<i>Caspase</i>-3, <i>Bax</i>, <i>Bcl</i>-2, and <i>Bcl</i>-<i>XL</i>) were observed. Proving that <i>Pe</i>Trx2 rapidly responded to Cd stress and played a vital role in mitigating Cd-induced oxidative stress and apoptosis. Our study demonstrated that <i>Pe</i>Trx2 is a key factor for <i>P. esculenta</i> to endure the toxicity of Cd, providing foundational data for further exploration of the molecular mechanisms underlying heavy metal resistance in <i>P. esculenta</i>.