Effects of the organophosphorus pesticide Folisuper 600 (methyl parathion) on the heart function of bullfrog tadpoles, Lithobates catesbeianus (Shaw, 1802) / Efeitos do pesticida organofosforado Folisuper 600 (metil paration) sobre a função cardíaca de girinos de rã-touro, Lithobates catesbeianus (Shaw, 1802)

Abstract The aim of this work was to evaluate whether the heart function of bullfrog tadpoles (25 Gosner stage) is affected by their acute exposure (48 h) to a sub-lethal concentration (10 µg.L–1) of the active principle of the organophosphorus pesticide Folisuper 600R (methyl parathion - MP). Our results demonstrated that MP causes not only a reduction in tadpoles’ cardiac ventricular mass, resulting in a marked reduction in their cardiac twitch force, but also impairs their swimming performance, irrespective of increasing their heart rate. Together, these findings indicate that low and realistic concentration of MP have a negative impact on tadpoles’ performance, jeopardizing their survival.

Resumo O objetivo do presente estudo foi avaliar se a função cardíaca de girinos de rãs-touro (estágio 25 de Gosner) é afetada pela exposição aguda (48h) a uma concentração sub-letal (10 µg.L–1) do princípio ativo do pesticida organofosforado Folisuper 600R (metil paration – MP). Nossos resultados demonstraram que o MP ocasionou não apenas uma redução na massa ventricular cardíaca dos girinos, como também provocou uma redução na sua força de contração cardíaca e de seu desempenho natatório, a despeito de ter sido observado um aumento de sua freqüência cardíaca. Conjuntamente, os achados aqui obtidos indicam que uma baixa e realística concentração de MP exerce um impacto negativo sobre o desempenho dos girinos, ameaçando sua sobrevivência.

Biochemical effects of some organophosphorus pesticides on the ovaries of albino rats.

An evaluation of the toxic effects of three organophosphates; monocrotophos, dimethoate and methyl parathion on female reproduction was made by biochemical estimations of cytoplasmic and membrance bound proteins, lipids, phospholipids and cholesterol in the rat ovaries after treatment with their low residual level doses (LD50 1/8-1/5) to three groups of six rats each for 90 days. All the three pesticides caused degenerative changes in the ovaries as evidenced by a significant decrease in the concentration of cytoplasmic as well as membrane bound proteins, total lipids, phospholipids and cholesterol. The observations are thus indicative of the reproductive toxicity caused by organophosphates at cellular and molecular level in the ovaries of rats.

Enzymatic changes induced by some organophosphorus pesticides in female rats.

An evaluation of toxic effects of three organophosphorus pesticides viz. monocrotophos, methyl parathion and dimethoate given orally daily for 90 days was done in terms of enzymatic changes in plasma and liver of female albino rats. A significant decrease was observed in the level of esterases in plasma with all the three pesticides. The activity of acid and alkaline phosphatases and aminotransferases increased significantly in plasma and significantly or marginally in liver with these pesticides. The results are thus indicative of the cellular toxicity of these organophosphates even after their subchronic administration in low doses for a long period.

Short-term and long-term survival studies in Rana tigrina tadpoles with reference to methyl parathion toxicity.

Toxicity of methyl parathion was studied on survival of Rana tigrina tadpoles. The LC50 values for short-term (upto 96 h) and long term studies (hatching to froglet) were determined. The LC50 values for 96 h and the total larval period were 4.36 and 1.30 ppm respectively. The toxicity of methyl parathion enchanced in relation to increase in concentration and duration. Teratological defects such as scoliosis and failure in emergence of fore limb were noticed. Safe levels were calculated for short-term (0.1 ppm) and long-term (0.03 ppm) studies. The present work stresses the neccessity of long term study especially for the developing amphibians.

Methyl parathion induced alterations in monoaminergic system of developing rat pups.

Methyl parathion induced alterations in the level of monoamines, viz. norepinephrine, dopamine and serotonin were studied in discrete regions of developing central nervous system of rat pups. A significant decrease in the level of monoamines noticed in methyl parathion toxicosis may be related to the altered neuronal activity and inefficiency, leading to depression and impairment in various behavioural activities. In contrast to AChE inhibition, monoamine oxidase (MAO) activity showed an increasing trend and it could cause deamination of catecholamines and accumulation of its metabolites. This suggests that an increased AChE inhibition may indirectly stimulate MAO activity in developing rat pups exposed to methyl parathion.

Effect of methyl parathion on Na(+)-K+ and Mg2+ adenosine triphosphatase activity in developing central nervous system in rats.

Developing rat pups exposed to sublethal doses of methyl parathion exhibit marked alteration in the activities of Na(+)-K+ and Mg2+ ATPases. The results suggest that the first post natal week developing animals are more sensitive to organophosphorous insecticide compared to higher age group animals.

Methyl parathion induced alterations in GABAergic system during critical stage of central nervous system development in albino rat pups.

Sublethal doses of methyl parathion (o, o-dimethyl-o-nitrophenyl thiophosphate) injected intraperitoneally to 7th day old developing albino rat pups induced alterations in the inhibitory GABAergic system of CNS. A substantial simulation of the inhibitory system was noticed. A profound increase was found in the level of the inhibitory transmitter, GABA on methyl parathion injection. An increase in the activity levels of the enzymes glutamic acid decarboxylase and 4-aminobutyrate-2-oxoglutarate-amino transferase in the cortex, brain stem and spinal cord of the CNS was found. It is observed that methyl parathion causes potentiation of the inhibitory transmission (GABAergic system) in the wake of inducing suppression of cholinergic system in CNS of developing rat pups.