Molluscs have long been regarded as promising bioindicator and biomonitoring subjects for heavy metals as molluscs are highly tolerant to heavy metals and exhibit high accumulation in their body. In spite of several previous studies about the impact of cadmium on molluscs, little information exists in literatures concerning the toxic effects of cadmium on Lymnaea acuminata, especially pertaining to behavioral and hematological changes as these are considered effective bioindicators and biomonitoring variables for detecting heavy metals in polluted water bodies. In the present study, the median lethal concentrations of cadmium chloride to snail, Lymnaea acuminata, were estimated to be 9.66, 7.69, 6.26, and 5.54 mg/L at 24, 48, 72, and 96 h, respectively. For behavioral studies, variable test concentrations of cadmium from 0.00 to 10 mg/L were used. The clumping tendency, crawling activity, and touch reflex in the exposed snails were gradually decreased with higher concentrations at 72 and 96 h. For measuring the hemocyte numbers in the circulating hemolymph of snail during chronic cadmium exposure, two sublethal doses of cadmium (10 and 20% 96-h LC-0.55 and 1.11 mg/L, respectively) were used. A significant variation (p < 0.05) from the control at all exposure times (7, 14, 21, and 28 days) was recorded at 1.11 mg/L concentration. The total count of circulating hemocytes was significantly reduced (p < 0.05) compared to the controls at both concentrations of cadmium exposure at all time periods except 14 and 21 days exposure at 0.55 mg/L where values were non-significantly increased. In comparison between two sublethal doses, blood cells were significantly (p < 0.05) lowered at 1.11 mg/L cadmium treatment. Considering the behavioral and hematological data, it seems possible to forecast the physiological state of snails in cadmium-contaminated water bodies and these findings can be used in determining the safe disposal level of cadmium in aquatic ecosystem.

Diazinon exposures have been linked to the onset of toxic pathways and adverse outcomes in aquatic species, but the ecological implications on model species are not widely emphasized. The objective of this study was to determine how the organophosphate pesticide diazinon affected hematological (hemoglobin, total red blood count, total white blood count, and mean corpuscular hemoglobin), growth (condition factor, hepatosomatic index, specific growth rate), biochemical (total serum glucose, total serum protein), and endocrine (growth hormone, tri-iodothyronine, and thyroxine) parameters in Clarias batrachus after chronic exposure. Diazinon was administered at predefined exposure doses (0.64 and 1.28 mg/L) and monitored at 15, 30, and 45 days into the investigation. Observation for most biomarkers revealed patterns of decreasing values with increasing toxicant concentration and exposure duration. Correlation analysis highlighted a significant inverse relationship between variables (mean corpuscular hemoglobin, condition factor, specific growth rate, tri-iodothyronine, thyroxine, and total serum protein) and elevated chronic diazinon exposure concentrations. The integrated indices (IBR and BRI) indexes were used to provide visual and understandable depictions of toxicity effects and emphasized the relativity of biomarkers in terms of sensitivity and magnitude or severity of responses under graded toxicant exposures. The significant damage reflected by evaluated parameters in diazinon exposure groups compared to control portends risks to the health of local fish populations, including Clarias batrachus in aquatic systems adjacent to agrarian landscapes.

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Nickel is a potential neurotoxic pollutant inflicting damage in living organisms, including fish, mainly through oxidative stress. Previous studies have demonstrated the impact of nickel toxicity on mitochondrial function, but there remain lacunae on the damage inflicted at mitochondrial respiratory level. Deficient mitochondrial function usually affects the activities of important adenosinetriphosphatases responsible for the maintenance of normal neuronal function, namely Na+K+ATPase, as explored in our study. Previous reports demonstrated the dysfunction of this enzyme upon nickel exposure but the contributing factors for the inhibition of this enzyme remained unexplored. The main purpose of this study was to elucidate the impact of nickel neurotoxicity on mitochondrial respiratory complexes and Na+K+ATPase in the piscine brain and to determine the contributing factors that had an impact on the same. Adult Clarias batrachus were exposed to nickel treated water at 10% and 20% of the 96 h LC50 value (41 mg.l–1) respectively and sampled on 20, 40 and 60 days. Exposure of fish brain to nickel led to partial inhibition of complex IV of mitochondrial respiratory chain, however, the activities of complex I, II and III remained unaltered. This partial inhibition of mitochondrial respiratory chain might have been sufficient to lower mitochondrial energy production in mitochondria that contributed to the partial dysfunction of Na+K+ATPase. Besides energy depletion other contributing factors were involved in the dysfunction of this enzyme, like loss of thiol groups for enzyme activity and lipid peroxidation-derived end products that might have induced conformational and functional changes. However, providing direct evidence for such conformational and functional changes of Na+K+ATPase was beyond the scope of the present study. In addition, immunoblotting results also showed a decrease in Na+K+ATPase protein expression highlighting the impact of nickel neurotoxicity on the expression of the enzyme itself. The implication of the inhibition of mitochondrial respiration and Na+K+ATPase dysfunction was the neuronal death as evidenced by enhanced caspase-3 and caspase-9 activities. Thus, this study established the deleterious impact of nickel neurotoxicity on mitochondrial functions in the piscine brain and identified probable contributing factors that can act concurrently in the inhibition of Na+K+ATPase. This study also provided a vital clue about the specific areas that the therapeutic agents should target to counter nickel neurotoxicity.

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