Oxidative stress in freshwater fish, Labeo rohita as a biomarker of malathion exposure.

This study examined the effect of lethal (4.5 µg/l) and sublethal (0.45 µg/l) malathion levels on oxidative stress responses of the freshwater edible fish, Labeo rohita. Fish were exposed to lethal (1-4 days) and sublethal (1, 5, 10, and 15 days) periods. In the present study, catalase and protease activity, hydrogen peroxide, malondialdehyde, protein carbonyls, and free amino acids levels increased in the gill, liver, and kidney tissues of fish exposed to lethal and sublethal concentrations of malathion except protein content. Time- and concentration-dependent induction/reduction of the above parameters by lethal and sublethal concentrations of malathion was observed in the tissues (the gill, liver, and kidney) of L. rohita. Thus, the results clearly infer oxidative damage and decline in antioxidant defense due to malathion-induced oxidative stress.

Behavioral and morphological endpoints: as an early response to sublethal malathion intoxication in the freshwater fish, Labeo rohita.

A short-term definitive test by the static renewal bioassay method was conducted to determine the acute toxicity (LC(50)) of commercial-grade organophosphate insecticide, malathion (50% EC) on the freshwater fish, Labeo rohita. Carp fingerlings were exposed to different concentrations of malathion for 96 hours. The acute toxicity (LC(50)) of malathion was found to be 4.5 microg/L. One tenth (1/10, 0.45 microg/L) of the acute toxicity value was selected as the sublethal concentration for subacute studies. The fish were exposed to sublethal concentration for 1, 5, 10, and 15 days and allowed to recover in toxicant-free medium for 15 days. Behavioral responses and morphological deformities were studied in the experimental tenures. Fish in toxic media exhibited irregular, random, circular swimming movements, hyperexcitability, loss of equilibrium, and sinking to the bottom. Caudal bending was the prime morphological malformation. The behavioral and morphological deformities were due to inhibition of acetylcholinesterase (AChE) activity. Inhibition of AChE activity results in excess accumulation of acetylcholine in cholinergic synapses, leading to hyperstimulation and cessation of neuronal transmission (i.e., paralysis). The carp were found under stress, but mortality was insignificant at the sublethal concentration tested. Impaired behavioral responses and morphological deformities were observed during recovery. This may be a consequence due to inhibition of brain and muscular AChE by malaoxon, via the biotransformation of sequestered malathion.

Gas-liquid chromatography for fenvalerate residue analysis: in vivo alterations in the acetylcholinesterase activity and acetylcholine in different tissues of the fish, Labeo rohita (Hamilton).

The disruption of acetylcholinesterase activity (AChE) in the freshwater fish, Labeo rohita is demonstrated in the present study using acetylthiocholine iodide as substrate. L. rohita on exposure to lethal (6 microg/L) and sub-lethal (0.75 microg/L) concentrations of fenvalerate showed time- and dose-dependent inhibition in the activity of AChE, suggesting a decrease in the cholinergic transmission and consequent accumulation of acetylcholine (ACh) in the tissues (brain, gill, liver, and muscle) leading to continuous nerve impulses, causing prolonged muscle contraction which, as a consequence, causes paralysis and results in death. These also have lead to behavioral changes and create widespread disturbance in the normal neural physiology of the fish. Residue analysis using a gas-liquid chromatography technique (GLC) revealed that highest quantity of fenvalerate accumulated in gill followed by liver and muscle under lethal concentrations, whereas in sub-lethal concentrations muscle accumulated the highest concentration followed by gill and liver. The results suggest that in a biomonitoring program AChE activity can be a good diagnostic tool for assessing fenvalerate toxicity. The lipophilic nature of fenvalerate is of concern, since L. rohita is an important staple fish species, which may lead to the phenomenon of biomagnification.

Behavioral and respiratory dysfunction in the freshwater fish, Labeo rohita (Hamilton) under malathion intoxication.

A short term definitive test by static renewal bioassay method was conducted to determine the acute toxicity (LC50) of the commercial grade organophosphate insecticide malathion (50% EC) in the freshwater edible fish, Labeo rohita. Carp fingerlings were exposed for 96 h to different concentrations (6.0 to 10.1 microL/L) of malathion. The acute toxicity value was found to be 9.0 microL/L and one tenth of LC50 (0.9 microL/L) was selected for sub acute studies. Behavioral patterns and oxygen consumption were studied in lethal (1, 2, 3, and 4 d) and sublethal concentrations (1, 5, 10, and 15 d). Carp in toxic media exhibited irregular, erratic, and darting swimming movements, hyperexcitability, and loss of equilibrium and sinking to the bottom, which might be due to the inactivation of acetylcholine esterase activity, resulting in excess accumulation of acetylcholine in cholinergic synapses leading to hyperstimulation. Variation in oxygen consumption (70.39% to 80.50%/4.45% to 21.35%) was observed in both lethal and sublethal concentrations of malathion, respectively. Such alterations in oxygen consumption may be due to respiratory distress because of impairment in oxidative metabolism. Fish at sub lethal concentrations were found under stress, but that was not fatal.