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Developmental stage determines the microplastic-induced disruption of antioxidant and DNA damage regulatory mechanisms in Oreochromis niloticus
Summary
Researchers exposed Nile tilapia (Oreochromis niloticus) at two developmental ages to microplastics and found that younger juveniles (48 days old) suffered a progressive collapse of their antioxidant defenses and significant DNA damage, while older juveniles (72 days old) stayed largely unharmed. The findings show that early life stages are far more vulnerable to microplastic toxicity, which should be factored into environmental risk assessments for aquatic species.
This investigation identifies a critical, age-dependent vulnerability to microplastic (MP) toxicity in Oreochromis niloticus.Juveniles at 48 days post-fertilization (dpf) exhibited a severe, time-dependent pathological progression, unlike resilient 72 dpf fish.In 48 dpf individuals, MP exposure initiated significant oxidative stress, indicated by a sustained 3.80fold upregulation of SOD1.This was followed by a transcriptional collapse of key peroxidedetoxifying enzymes, with catalase (CAT) and glutathione peroxidase (GPx) expression falling significantly below baseline after 72 hours.The consequent antioxidant system failure precipitated a potent genotoxic response, evidenced by a delayed yet dramatic upregulation of the DNA damage marker Gadd45bb.In contrast, 72 dpf fish maintained homeostatic expression of CAT, GPx, and Gadd45bb, showing only a moderate SOD1 induction.These findings delineate a distinct cascade from acute oxidative stress to antioxidant failure and significant DNA damage that is exclusive to early developmental stages.This work underscores the necessity of incorporating developmental stage and prolonged exposure durations into environmental risk assessments for microplastics in aquatic ecosystems.