Evaluation of cadmium toxicity in Penaeus monodon using ecotoxicological tools: A foundational step for deriving...

Developing accurate and comprehensive water quality criteria for contaminants is crucial for the effective management and conservation of coastal ecosystems. This study seeks to generate key ecotoxicological data, such as the median lethal concentration (LC₅₀), No Observed Effect Concentration (NOEC), and Lowest Observed Effect Concentration (LOEC) for cadmium (Cd), to support the formulation of site-specific water quality standards tailored to marine and coastal environments. Such data serve as fundamental building blocks for water quality regulations. Post-larvae of Penaeus monodon were acclimated and exposed to varying Cd concentrations under controlled conditions. The acute toxicity endpoint (96-hour LC₅₀) was assessed using mortality data, while the chronic toxicity endpoints (NOEC, LOEC, and chronic value) were determined based on the percentage survival recorded during the exposure period. Biomarker responses, including antioxidant enzyme activity, lipid peroxidation, energy reserves, and cellular energy allocation, were analyzed, which serve as strong supportive evidence of toxicity at the tested exposure concentrations. The LC₅₀ of Cd for Penaeus monodon was 1.86 ± 0.12 mg L^-1, with upper and lower confidence intervals of 1.31 to 2.37 mg L^-1, respectively. The NOEC, LOEC, and chronic value observed were 0.17, 0.27, and 0.22 mg L^-1, respectively. Antioxidant enzyme activities, including superoxide dismutase, catalase, glutathione S-transferase, and glutathione peroxidase, exhibited significant dose-dependent increases. Lipid peroxidation levels also increased. Energy reserves (proteins, carbohydrates, lipids) declined significantly, while bioenergetic markers and electron transport system activity increased. Cellular energy allocation showed a notable decline. Eye histology revealed structural damage, including necrosis and detachment of cone cells from retinular cell layers at higher Cd concentrations. Integrated Biomarker Response analysis highlighted oxidative stress as a primary response mechanism, with glutathione peroxidase and lipid peroxidation being the most sensitive indicators.