Effect of ferrous sulphate on aspartate and alanine aminotransferases of brain of Tilapia mossambica.

Iron in the form of ferrous sulphate coming from sources such as mines, writing inks, blue pigments, dyeing industries, photography, medicine, deodorizers, disinfectants, fungicides and molluscides, etc. contributes in elevating ferrous sulphate of water bodies. The present study investigated the action of ferrous sulphate on the local fish Tilapia mossambica. Tilapia exposed to 0.001 g/L ferrous sulphate for 30 days showed reduction of cytosolic AST and ALT activities of cerebral cortex by 35.4% and 29.1%, respectively, while exposure to 0.01% ferrous sulphate promoted 49.2% and 38.4% reduction of AST and ALT activities. Similarly mitochondrial AST and ALT activities reduced by 50% and 34.8%, respectively, on exposure to 0.001 g/L ferrous sulphate while 0.01 g/L ferrous sulphate promoted 51% and 47.8% reductions of AST and ALT activities at the end of 30 days, suggesting interference in the glutamate and protein metabolism of Tilapia brain.

Aspartate aminotransferase and alanine aminotransferase activities of rat brain during crush syndrome.

Crush syndrome develops due to muscle crush injury often found in patients extricated from prolonged compression after disasters. It leads to rhabdomyolysis, kidney failure and hypovolemic shock, followed by decreased blood supply, to tissue under compression and general body parts including brain. In the present study, experimental model of crush syndrome in albino rats was induced by, 2h of compression followed by 48 h of decompression, of femoral muscle tissue. Aspartate and alanine aminotransferase activities of rat brain regions during crush syndrome were investigated. After exposure to 2h compression in comparison to normal/control levels, both cytosolic AST and ALT activities reduced. Cytosolic AST activity reduced by 31.2%, 26.1% and 19.4% in olfactory lobes, cerebral cortex and cerebellum, respectively, whereas cytosolic ALT activity decreased by 51.1%, 52.4%, 47.4% and 36.9% in olfactory lobes, cerebral cortex, cerebellum and medulla oblongata, respectively.

The study of Na+, K(+)-ATPase activity of rat brain during Crush syndrome.

Crush syndrome (CS) results from severe traumatic damage to the organism that is characterized by stress, acute homeostatic failure of the tissues, and myoglobinuria with severe intoxication. This leads to an acute impairment of kidneys and heart. The peripheral and central nervous systems are also the subject of significant changes in CS. Na(+), K(+)-ATPase is a critical enzyme in neuron that is essential for the regulation of neuronal membrane potential, cell volume as well as transmembrane fluxes of Ca(++) and Excitatory Amino Acids. In the present study, Na(+), K(+)-ATPase activity of rat brain regions [Olfactory lobes (OL), Cerebral cortex (CC), Cerebellum (CL), and Medulla oblongata (MO)] during CS was investigated. Experimental model of CS in albino rats was induced by 2-h of compression followed by 2, 24, and 48-h of decompression of femoral muscle tissue. In this study, we have observed elevation in Na(+), K(+)-ATPase activity above normal/control levels in all parts of brain (OL: 34.4%; CC: 1.0%; CL: 3.3% and MO: 45%) during 2-h compression in comparison to controls.