RESUMEN
Heavy infestation by Perna viridis has been observed in the sub-seabed seawater intake tunnel and CWS of a tropical coastal power station in-spite of continuous low dose chlorination regime (0.2 ± 0.1 mg L-1) (CLDC), indicating periodical settlement and growth. Continuous arrival of mussels (colonized in the sub seabed tunnel intake section) at the pump house indicated that the mussels were able to tolerate and survive in a chlorinated environment, for varying time periods and were dislodged when they become weak and subsequent death, leading to flushing out of the system. In the present study, effect of continuous chlorination [0.2 mg L-1 (in-plant use); 0.5 mg L-1 (shock dose) & 1.0 mg L-1 (high levels)] was evaluated on mussels to assess; (a) time taken for mortality, (b) action of chlorine on physiological, genetic, metabolic and neuronal processes. 100% mortality of mussels was observed after 15 (0.2 mg L-1); 9 (0.5 mg L-1) and 6 days (1.0 mg L-1) respectively. Extended valve closure due to chlorination resulted in stress, impairing the respiratory and feeding behavior leading to deterioration in mussel health. Pseudofaeces excretion reduced to 68% (0.2 mg L-1); 10% (0.5 mg L-1) and 89% (1.0 mg L-1) compared to controls. Genotoxicity was observed with increase in % tail DNA fraction in all treatments such as 86% (0.2 mg L-1); 76% (0.5 mg L-1) and 85% (1.0 mg L-1). Reactive Oxygen Species (ROS) stress biomarkers increased drastically/peaked within the first 3 days of continuous chlorination with subsequent quenching by antioxidant enzymes. Gill produced highest generation of ROS; 38% (0.2 mg L-1); 97% (0.5 mg L-1); 98% (1.0 mg L-1). Additionally, it was shown that 84% (0.2 mg L-1), 72% (0.5 mg L-1), and 80.4% (1.0 mg L-1) of the neurotransmitter acetylcholinesterase activity was inhibited by chlorine at the nerve synapse. The cumulative impact of ROS generation, neuronal toxicity, and disrupted functions weakens the overall health of green mussels resulting in mortality.
