Biochemical effects of ethanol on oreochromis mossambicus (Peters)

The present study dealt with the haematological, biochemical and istopathological impacts of different sub lethal concentrations of ethanol on a euryhaline teleost Oreochromis In05.s‘ambicu.5' (Peters).Studies carried out using GC indicated an increase in blood ethanol oncentration of the fish which mainly arose due to fishes entering into a state of hypoxia which explains ethanol production as an ubiquitous “anaerobic” end product, which gets accumulated whenever metabolic demand exceeds the mitochondrial oxidative potential. The very low amount of ethanol detected in the control group ofO mossambicns was mainly due to the activity of microorganisms in the gut ofO. Nzossambicus.Oedcma observed in the present study, is a defense mechanism that reduces the branchial superficial area of the fish which comes in contact with the external milieu. These mechanisms also increase the diffusion barrier to the pollutant. Dilation of the blood vessels is due to increased permeability helping in the free passage of ethanol into the blood stream. Telangiectasis observed explains the state of asphyxia of the fish when subjected to ethanol toxicity indicating acute respiratory distress. Gill aneurysm observed indicates impaired respiratory function. This is related to the rupture of the pillar cells which results in an increased blood flow inside the lamellae, causing dilation of the blood vessel or even aneurysm of gill.The present findings warrant future studies to explore A'T'Pases as possible biomarkers of pollutant exposure in ecotoxicology. This study indicated that O. mossambicus when exposed for 7 and 21 days to ethanol was under tremendous stress and parameters employed in this study can be adapted for future investigations as biomarkers of damage caused by ethanol to aquatic organisms. The present study revealed that O. mossambicus is sensitive to sub lethal concentrations of ethanol.

Withania somnitera and withanolide a mediated restoration of AMPA and NMDA receptor function in pilocarpine induced temporal lobe epilepsy

The onset of spontaneous seizures triggers a cascade of molecular and cellular events that eventually leads to neuronal injury and cognitive decline. The present study investigated the effect of Withania somnifera (WS) root extract and Withanolide A (WA) in restoring behavioural deficit by inhibiting oxidative stress induced alteration in glutamergic neurotransmission. The subdued performance in behavioural tests shows impaired motor coordination and memory. Histopathological investigations revealed significant neuronal loss in hippocampus of epileptic rats indicating glutamate mediated excitotoxicity. The treatment with WS and WA restored behavioural deficit and ameliorated neuronal loss. An altered redox homeostasis leading to oxidative stress is a hallmark of TLE. The antioxidant potential was afflicted in epileptic rats, evident from altered activity of SOD and CAT, down regulation of SOD and GPX expression and enhanced lipid peroxidation. The antioxidant property of WS and WA restored altered antioxidant capacity. Alteration in GDH activity and down regulation of GLAST expression resulted in enhanced glutamate content in the brain regions. The metabolism of glutamate was altered in the form of down regulated GAD expression. The alteration in synthesis, transport and metabolism resulted in further increase of the glutamate concentration at the synapse leading to glutamate mediated excitotoxicity. The decreased NMDA and AMPA receptor binding and down regulated NMDA R1, NMDA 2B and AMPA (GluR2) mRNA expression indicated altered glutamergic receptor function. The treatment with WS and WA reversed altered glutamergic receptor function, synthesis, transport and metabolism. The enhanced levels of second messenger IP3 responsible for Ca2+ mediated toxicity was reversed after treatment with WS and WA. Neurotoxics concentration of glutamate resulted in up regulation of pro apoptotic factors Bax and Caspase 8 and down regulation of anti apoptotic factor Akt resulting in neuronal death. The treatment with WS and WA resulted in activation of Akt and down regulation of Bax and caspase 8 leading to blocking of apoptotic pathway. The treatment with WS and WA resulted in reduced seizure frequency and amelioration of associated alterations suggesting the therapeutic role of Withania somnifera in temporal lobe epilepsy