Response of Cyprinus carpio (Linn) to sublethal concentration of cypermethrin: alterations in protein metabolic profiles

Freshwater fish, Cyprinus carpio were exposed to sublethal concentration (1.2 microg l(-1)) of cypermethrin for 6, 12, 24 and 48 h to analyze various parameters of protein metabolism in functionally different tissues. Total, structural and soluble proteins showed decrement; where as free amino acids and the activities of protease, aspartate aminotransferase and alanine aminotransferase significantly increased in cypermethrin exposed fish. Interestingly, ammonia content decreased but urea and glutamine increased at all periods of exposure. It was also observed that alterations steadily increased with the period of exposure and exhibited tissue specificity. Thus variation in the protein metabolism of the fish exposed to cypermethrin indicates its toxic effect on the cellular metabolism thereby leading to impaired protein synthetic machinery.     

Nickel induced changes on some aspects of protein metabolism in the tissues of Pila globosa

Some aspects of protein metabolism were studied in foot, hepatopancreas and mantle tissues of snail, Pila globosa on exposure to lethal concentration for 2 days (336.7 mg/L) and sublethal concentration (67.34 mg/L) of nickel for 1, 5 and 10 days. Total, structural and soluble proteins decreased significantly and to continence, this the levels of amino acids and protease activity increased in all the tissues of snail at all time points examined. Activities of AAT (Aspartate aminotransferase) and AlAT (Alanine aminotransferase) showed contrasting trends of inhibition and elevation during lethal and sublethal concentrations of nickel treatment. GDH (Glutamate dehydrogenase) activity was increased in all the tissues with increase in exposure time. Level of ammonia decreased in snails at sublethal concentration, but increment was observed in lethal concentration along with increased urea content. Under lethal and sublethal exposures, the changes in all the parameters were more pronounced in hepatopancreas followed by foot and mantle. At most instances, snails in the lethal medium were affected more compared to sublethal concentration.     

Gas–liquid chromatography for fenvalerate residue analysis: alterations in the ionic concentration and associated adinosine triphosphatases in fish,Cirrhinus mrigala (hamilton)

In the present study, an attempt has been made to quantify the fenvalerate accumulated in different tissues (gill, muscle and liver) and observe changes involved in the levels of sodium, potassium and calcium ions and Na⁺–K⁺, Mg²⁺ and Ca²⁺ adenosine triphosphatase (ATPase) activities in the freshwater fish, Cirrhinus mrigala on short-term and long-term exposure to the median lethal and sublethal concentration of fenvalerate. Residue analysis using gas–liquid chromatography (GLC) technique revealed that fenvalerate accumulated in highest quantity in gill followed by liver and muscle under median lethal concentration (6?µg?L^?1). Whereas in sublethal concentration (0.6?µg?L^?1), muscle accumulated highest quantity followed by gill and liver, which might be due to the fact that fenvalerate is highly lyphophilic. The ion concentration and ATPase activity were found effected in fish exposed to lethal and sublethal concentrations of fenvalerate. Concentration of Na⁺, K⁺ and Ca²⁺ ions decreased in gill, muscle and liver on being exposed to median lethal concentration to a significant level. Whereas the changes were not highly pronounced at sub lethal level indicating low concentration of fenvalerate and its non-toxic effect at chronic exposure. Na⁺–K⁺, Mg²⁺ and Ca²⁺ ATPases activity were also found decreased in correspondence to the ionic change under median lethal and sub lethal concentrations in target tissues. This might have lead to behavioural changes and create wide-spread disturbance in the normal physiology, ultimately causing the death of the fish. The results suggest that in biomonitoring programmes, ions and associated ATPases can be a good diagnostic tool for fenvalerate toxicity.