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Objective: To evaluate the hepatoprotective activity of aqueous extract of Oxalis debilis Kunth in carbon tetrachloride (CCl 4 )-induced hepatotoxicity in Swiss albino mice.Methods: Hepatotoxicity was induced by CCl 4 30% in olive oil (1 ml/kg intraperitoneally). Mice were treated with aqueous extract of O. debilis at doses of 250 and 500 mg/kg body weight orally for 14 days. There were two groups, pre-treatment (once daily for 14 days before CCl 4 intoxication) and post-treatment (2, 6, 24, and 48 hrs after CCl 4 intoxication). The observed effects were compared with a known hepatoprotective agent, silymarin.Results: Pre-treatment and post-treatment groups of aqueous extract of O. debilis significantly reduced elevated serum levels of serum transaminases, alkaline phosphatase, and bilirubin and increased the level of total protein as compared to CCl 4 -treated group. The histopathological study also confirms the hepatoprotection. Preliminary qualitative phytochemical analysis of the plant revealed the presence of phenolic compounds, tannins, flavonoids, and saponins. Conclusion:The results of this study suggest that O. debilis can be used as safe, cheap, and alternative preventive and protective drugs against liver injury. The protective effect observed could be attributed to the presence of various phytochemicals which are responsible for the restoration of liver damage.

Glutamate (Glu) is a major excitatory aminoacid neurotransmitter in the mammalian brain. Under Certain Circumstances Glu can also exert toxic effects on neuronal Cells. To unravel the biochemical mechanisms of Glu‐induced acute neuronal injury, Glu 1μmol/1μl was microinjected into cerebral Cortex, striatum and hippocampus of adult rats and oxidative stress and antioxidant parameters were evaluated. The results show that the rate of lipid peroxidation was significantly increased in the above brain regions following Glu administration suggesting neuronal membrane damage and also the total and free sulfhydryl groups were significantly depleted, indicating altered red‐ox status of the cells. There was also alteration in the activity of antioxidant enzyme catalase in cerebral cortex. Some of the above Glu‐induced effects were reversed or modified by NMDA receptor antagonist MK‐801.

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Glutamate (glu) an excitatory neurotransmitter amino acid, is present in high concentrations in the mammalian central nervous system and is the most abundant amino acid in our daily diet. In the present study the activities of lactate dehydrogenase (LDH) and glutamate dehydrogenase (GDH) were evaluated in the circumventricular organs (CVO) of the brain in 25-day-old rats following MSG administration at a dose of 4 mg/g b.wt during the first ten days of life. The results show the LDH activity increased to 265% of that in the control (p < 0.001), whereas GDH activity was significantly decreased (p < 0.05). The great elevation in LDH, a cytoplasmic marker enzyme, is apparently due to cytoskeletal changes brought about as a consequence of glu toxicity, whereas lowered GDH activity indicates altered glu homostasis in the blood-brain-barrier deficient areas following neonatal exposure to glu.

The present study aims to assess the harmful ^ect of a selected medidnalplarit extract on albino mice and I investigate its impact on its behavior and brafn enzymes. Here force iswm.test showed significantly dose ^ dependent increase immobility. But in case of /ocomofor acfjVity there found signiUcaht decrease in experimental.group. '4 Besides significant elevation of Lactate dehydrogenase activity and reduction of Catalase activity of brain was found, which * iT ^^c>M'^£'J•'^? "^gjfy£'£-fi:9j:tj:fth9e,rt.'-^f J.bs'rs'We; it €^i>e'assi/med that the Aktoniaschalsris extract has some barmM spcivea r'^s" "ego effect on mice br.

Objective: This study aims to assess the effects of the aqueous extract of Hydrocotyle javanica (HJ) in ameliorating mercury-induced neurobehavioral toxicity.Methods: For the study, 36 adult male Swiss albino mice of 25–30 g in weight were taken. They were equally divided into six groups. Group I was treated with distilled water, Group II was treated with mercuric chloride (1.5 mg/kg), Group III was treated with HJ extract low dose (100 mg/kg), Group IV was treated with HJ extract high dose (200 mg/kg), Group V was treated with mercuric chloride plus HJ extract low dose, and Group VI was treated with mercuric chloride plus TB extract high dose. In all the groups, the doses were administered orally through oral gavage tube and the treatment lasted for 14 days. The behavioral effects evaluated were locomotor activity in the open field test, immobility in forced swimming test and anxiety in elevated plus maze test, spatial learning ability, and memory in the Morris water maze test.Results: The present study showed that mercury exposure significantly decreased the locomotor activity (p<0.001), number of annulus crossovers (p<0.001), number of open arm entries (p<0.01), time spent in open arms (p<0.001), and increased escape latency (p<0.01), path length (p<0.001), and immobility (p<0.001) in mice. The aqueous extract of HJ significantly alleviated the neurotoxic effects of mercury. The aqueous extract of HJ showed to increase the locomotor activity (p<0.01), number of annulus crossovers (p<0.001), number of open arm entries (p<0.05), and time spent in open arms (p<0.05), which was decreased in mercury-exposed mice. The HJ extract also showed to decrease the immobility (p<0.001), escape latency (p<0.05), and path length (p<0.001) in mercury-exposed mice.Conclusion: The result of the study shows that neurobehavioral changes induced by mercuric chloride were significantly reversed by the aqueous extract of HJ. Thus, base on the present study, it is concluded that HJ is effective in ameliorating the neurobehavioral deficits induced by mercury.