Muniswamy David

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 (LC50) 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 (LC50) of malathion was found to be 4.5 µg/L. One tenth (1/10, 0.45 µg/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.

Cypermethrin induced: In vivo inhibition of the acetylcholinesterase activity in functionally different tissues of the freshwater teleost, Labeo rohita (Hamilton)

Effects of cypermethrin at different concentrations and exposure periods were investigated on the freshwater fish, Labeo rohita, to establish inhibitory effect of pesticide on acetyl cholinesterase (AChE) activity and associated behavioral changes. Fish were exposed to 1/7th (0.57 µg L−1) and 1/12th (0.33 µg L−1) of the lethal concentration (4 µg L−1) of cypermethrin for a period of 1, 7, or 14 days and allowed to recover for a further 7 days. Maximal inhibition in AChE activity in exposed fish was found in brain followed by muscle, gill, and liver on day 14 at both sublethal concentrations of cypermethrin. Recovery showed a rise in AChE activity but significantly decreased compared to controls. Depression of AChE activity suggests decreased cholinergic transmission and consequent accumulation of acetylcholine (ACh) in tissues leading to cessation of nerve impulses. This led to behavioral and morphological changes due to impaired neurophysiology in fish. Fish in toxic media exhibited erratic, and darting swimming movements, hyperexcitability, and loss of equilibrium and these symptoms persisted even during recovery.

Ultrastructural responses and oxidative stress induced by cypermethrin in the liver of Labeo rohita

The present study was conducted to establish the relationship between selected oxidative stress parameters and ultrastructural responses in liver tissue of Labeo rohita fingerlings exposed to cypermethrin. Fish were exposed to lethal (4.0 μg L−1) and sublethal (0.4 μg L−1) concentrations of cypermethrin for a period of 24, 48, 72 and 96 h for acute studies and 1, 5, 10 and 15 days for subacute studies, respectively. Results showed increased catalase (CAT) and protease activity, hydrogen peroxide (H2O2), malondialdehyde (MDA), protein carbonyls and free amino acid (FAA) levels at both concentrations. This suggests participation of free-radical-induced oxidative cell injury in mediating the hepatotoxicity of cypermethrin. In corroboration of this, ultrastructural lesions witnessed a reduction in the number of cell organelles, swollen, vacuolated and condensed mitochondria, dilated rough endoplasmic reticulum, and reduced numbers of smooth enodplasmic reticulum, peroxisomes and lysosomes at the lethal (4.0 μg L−1) concentration. At the sublethal (0.4 μg L−1) concentration, cytoplasmic vacuolation, condensed, vacuolated and swollen mitochondria, dilated rough endoplasmic reticulum and an absence of hepatocyte microvilli were prominent. Ultrastructural changes were exhibited as subcellular responses due to the imbalance in cellular oxidative status by means of oxidative damage.

Sodium cyanide-induced modulations in the activities of some oxidative enzymes and metabolites in the fingerlings of Cyprinus carpio (Linnaeus)

Carp fingerlings exposed to a sublethal concentration (0.5 mg L−1) of sodium cyanide showed a steady decrement over a 7-day period in respiratory rate, rise in lactate dehydrogenase (LDH), and fall in succinate dehydrogenase (SDH) activities followed by variations in lactic and pyruvate levels. Changes in these enzyme activities might be due to impaired oxidative metabolism and severe cellular damage leading to the release of these enzymes. Decline in the activities of SDH and LDH clearly represents a shift from aerobic to anaerobic metabolism as evidenced by elevated lactate and decline in pyruvate levels. The shift to anaerobic metabolism is also reflected by severe drop in the respiratory rate of the fish. This may be a consequence of the blockage of electron transfer from cytochrome c oxidase to molecular oxygen, thus ceasing cellular respiration and it can lead to cellular hypoxia even in the presence of normal hemoglobin oxygenation. Hence, we indirectly reconfirm the inhibition of oxidative metabolism by sodium cyanide. Alterations in behavioral pattern induced by sublethal sodium cyanide exposure may be due to the combination of cytotoxic hypoxia with lactate acidosis, which depresses the central nervous system (CNS); as the brain is the most sensitive site to anoxia, it results in impaired CNS function.

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 μg/L) and sub-lethal (0.75 μg/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.

Quinalphos Induced Alterations in the Levels of Ions and Whole Animal Oxygen Consumption of Freshwater Fish, Cyprinus Carpio (Linnaeus, 1758)

The fi ngerlings of Cyprinus carpio were exposed to the lethal concentration (7.5 g/l) of quinalphos (Emulsi fi ed Concentrate 25 percent) for 1,2,3 and 4 days respectively to study the levels and whole animal oxygen consumption. Exposed fi sh showed a signi fi cant decrease in the whole animal oxygen consumption due to the respiratory distress as a consequence of the impairment of oxidative metabolism. The ionic content of Na + , K + and Ca 2+ also decreased signi fi cantly in gill, liver and muscle tissue of exposed fi sh, signifying the altered cellular proliferation and deranged Na + , K + and Ca 2+ ionic pump due to probable consequence of tissue damage.