Protective effect of lemongrass oil against dexamethasone induced hyperlipidemia in rats: possible role of decreased lecithin cholesterol acetyl transferase activity

OBJECTIVE@#To evaluate the anti-hyperlipidemic activity of lemongrass oil against in dexamethasone induced hyperlipidemia in rats.@*METHODS@#Administration of dexamethasone was given at 10 mg/kg, sc. to the adult rats for 8 d induces hyperlipidemia characterized by marked increase in serum cholesterol and triglyceride levels along with increase in atherogenic index.@*RESULTS@#Lemongrass oil (100 and 200 mg/kg, po.) treatment has showed significant inhibition against dexamethasone hyperlipidemia by maintaining the serum levels of cholesterol, triglycerides and atherogenic index near to the normal levels and the antihyperlipidemic effect of the lemongross oil was comparable with atorvastatin 10 mg/kg, po. The possible mechanism may be associated with decrease in lecithin cholesterol acetyl transferase (LCAT) activity.@*CONCLUSIONS@#These results suggested that Lemon gross oil possess significant anti-hyperlipidemic activity.

Alloxan diabetes-induced oxidative stress and impairment of oxidative defense system in rat brain: neuroprotective effects of cichorium intybus

Diabetes mellitus impairs glucose homeostasis causing neurological disorders due to perturbation in utilization of glucose. The mechanisms responsible for failure of glycaemic control in diabetes need to be thoroughly elucidated and hence the present study was initiated. Diabetes was induced in albino rat models with alloxan monohydrate [40 mg/Kg intravenously]. Oxidative damage, impairment of oxidative defense and neuronal activity were investigated in cerebral hemispheres 48 h after alloxan administration. Diabetes caused an elevation [p < 0.001] of blood glucose, protein carbonyl content [PrC] and lipid peroxidation. The brain level of the antioxidant enzyme, catalase [CAT], reduced glutathione [GSH] and acetyl cholinesterase [AChE] exhibited significant decline in alloxan-diabetes. Feeding with dried powder leaves of Cihorium intybus decreased blood glucose level to near normal level. Impaired glucose metabolism in the brain was the key factor responsible for the elevated oxidative damage leading to brain dysfunction in diabetes

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.

Insecticide induced disruptions in functioning of developing brain of Rana cyanophlictis.

Synthetic pyrethroid insecticide permethrin significantly decreased the levels of regulatory proteins (S-100 and calmodulin) in the developing CNS of tadpoles of R. cyanophlictis. Remarkable inhibition of enzymes acetylcholinesterase and choline acetylase and significant accumulation of neurotransmitter acetylcholine were observed in permethrin treated animals. Permethrin exposure significantly decreased the activity of phosphodiesterase. The results support molecular disruptions occurring due to permethrin induced toxicity. This in turn may bring about neuronal inefficiency in the treated tadpoles.

Methyl parathion induced regional alterations in the regulatory proteins 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 15 and 21 day old rat pups induced regional alterations in the central nervous system (CNS) in the levels of total RNA, total proteins, modulatory protein Calmodulin (CaM), in the activity levels of membrane bound enzyme Ca(2+)-ATPase and phospholipids. Levels of RNA and total proteins increased considerably in 15 days old methyl parathion treated (MPT) rat pups. Contrary to this the RNA and total protein content exhibited remarkable decrease in 21 day old methyl parathion treated animals. Calmodulin level showed an increase in cerebral cortex and brain stem and decrease in cerebellum and spinal cord in 15 day old methyl parathion treated rat pups. Whereas the level of Calmodulin decreased in cerebral cortex and cerebellum and increased in brain stem and spinal cord in 21 day old methyl parathion treated rat pups. Activity levels of calcium dependent ATPase showed significant inhibition in all the regions of Central Nervous System (CNS) of 15 and 21 day old methyl parathion treated rat pups. Phospholipids showed a general increase in all the regions of Central Nervous System on methyl parathion exposure. In the light of these observations, it has been suggested that the molecular regulatory mechanisms involving Ca2+/CaM are rendered inefficient due to toxic impact of methyl parathion.