Comprehensive insights into the toxicological disruption of cadmium to juvenile Tachypleus tridentatus: From physiological impairments to multi-omics alterations.

Cadmium (Cd) is highly toxic to aquatic organisms. This study investigated the toxic effects and mechanisms of environmentally relevant Cd concentrations on juvenile Tachypleus tridentatus using physiological, biochemical, lipidomic, and transcriptomic analyses. After 28 days, 0.5 and 5 μg/L Cd significantly inhibited growth, reducing body weight and carapace width. This growth retardation was linked to biphasic molting dysregulation, with initial suppression and subsequent premature activation of chitinase and β-NAGase, disrupting the molting rhythm. Dynamic antioxidant responses were observed: SOD increased only in the 0.5 μg/L group at days 7 and 28, while CAT increased at day 7 but decreased at day 28 in both Cd treatments. The glutathione-dependent pathway was impaired, with no significant MDA elevation. Innate immunity showed a time-dependent pattern: ACP decreased at day 7 in the 5 μg/L group but increased at day 28 in both treatments; AKP increased at day 28 in both treatments; LZM increased at day 7 but decreased at day 28 in both treatments. Key immune-related genes (e.g., Dscam, PGRP-SC2, Ctsz) were downregulated. Lipidomics analysis revealed a global downregulation of core lipids, including triglycerides, diacylglycerols, phosphatidylcholines, and phosphatidylethanolamines, indicating disrupted lipid homeostasis and energy reserve utilization. Transcriptomic profiling further demonstrated that Cd exposure triggered the upregulation of defensive signaling pathways while concurrently downregulating genes associated with the cytoskeleton, cathepsins, and caspase-independent apoptosis, collectively impairing cellular homeostasis and immune function. These findings fill a critical knowledge gap in the ecotoxicological risk assessment of this ancient and endangered species under subchronic, low-level heavy metal exposure.