Effect of treatment of cow's urine "Gomutra" and antioxidants in alleviating the lindane-induced oxidative stress in kidney of Swiss mice (Mus musculus).

The study aimed to evaluate the effect of cow urine and combination of antioxidants against lindane induced oxidative stress in Swiss mice. Male healthy mice, 8-10 weeks old, weighing 30 ± 5 g were randomly selected and divided into eight groups, namely, control (C); lindane (L); antioxidant (A), antioxidant+lindane (A+L), cow urine (U), cow urine+lindane (U+L), cow urine+antioxidants (U+A) and cow urine+antioxidants+lindane (U+A+L). Group C animals were administered only the vehicle (olive oil); doses selected for other treatments were: lindane: 40 mg/kg b.w.; antioxidants: 125 mg/kg b.w. (vitamin C: 50 mg/kg b.w., vitamin E: 50 mg/kg b.w., α-lipoic acid: 25 mg/kg b.w.) and cow urine: 0.25 ml/kg b.w. In group A+L and U+L antioxidants and cow urine were administered 1 h prior to lindane administration and in group U+A and U+A+L cow urine was administered 10 min before antioxidants. All treatments were administered orally continuously for 60 days. Lindane treated group showed increased lipid peroxidation, whereas glutathione, glutathione peroxidase, superoxide dismutase, catalase, protein and endogenous levels of vitamin C and E were significantly decreased compared to control. Administration of cow urine and antioxidants alleviated the levels of these biochemical parameters.

Effect of pressure blanching on sensory and proximate composition of peanut milk.

Small scale process for the production of peanut milk was developed from M-522 variety of peanut. Three treatments i.e. traditional, 1% NaHCO3 soaking and pressure blanching (at 121 °C, 15 psi for 2, 3 and 5 mins) were given for the preparation of peanut milk. The milks so obtained were analyzed for chemical composition and also subjected to organoleptic evaluation using nine point hedonic scale by semi trained panel of judges. Peanut milk prepared by pressure blanching (at 121 °C, 15 psi for 3 min) was found most acceptable method. The proximate composition of the most acceptable peanut milk prepared by pressure blanching (at 121 °C, 15 psi for 3 min) was found to be moisture 88.22%, ash 0.16%, fat 1.65%, protein 3.27%, total solids 11.78%. Based on the results it was concluded that the pressure blanching was found most acceptable method for the preparation of peanut milk beverage although it had the negative effect on the protein and total solid extraction.

Modulation of acid phosphatase and lactic dehydrogenase in hexachlorocyclohexane-induced hepatocarcinogenesis in mice.

The present study was designed to elucidate the involvement of acid phosphatase (ACP) in metastasis and lactate dehydrogenase (LDH) as an immediate compensatory alleviation mechanism for energy stress in liver lesions induced by hexachlorocyclohexane in Swiss mice. Animals were continuously exposed to hexachlorocyclohexane (500 ppm) for 2, 4, and 6 months. Neoplastic nodules and tumors developed after continuous exposure for 4 and 6 months, respectively. The distribution pattern of both enzymes markedly varied in neoplastic nodules and tumors. Intense ACP activity was more observed only in sinusoids and blood vessels of neoplastic nodule, whereas an overall increase in ACP activity was observed in the tumor. Noticeably, a significant decline in LDH activity was noted after 2 and 4 months of exposure, whereas LDH in a tumor region showed intense enzymatic activity. The role of acid phosphate in metastasis and LDH in oxidative stress during hepatocarcinogenesis induced by hexachlorocyclohexane has been discussed.

Alleviation of lindane induced toxicity in testis of Swiss mice (Mus musculus) by combined treatment with vitamin C, vitamin E and alpha-lipoic acid.

Mitigation of lindane induced toxicity in testis of Swiss mice by combined treatment with vitamin C, vitamin E and alpha-lipoic acid has been evaluated. Male healthy mice (40), 8-10 weeks old were randomly selected and divided into 4 groups, control (C); lindane (L); antioxidant (A) and antioxidant plus lindane (A+L). Group C animals were administered only the vehicle (olive oil); in group L lindane was administered orally at a dose of 40 mg/kg body wt.; in group A combination of antioxidants at a dose of 125 mg/kg body wt.(vitamin C: 50 mg/kg body wt., vitamin E: 50 mg/kg body wt. and alpha-lipoic acid: 25 mg/kg body wt.) was administered orally; in group A+L both antioxidants (125 mg/kg body wt.) and lindane (40 mg/kg body wt.) were administered at their respective doses. In group A+L antioxidants were administered 1 h prior to lindane administration. All treatments were continuously given for 60 days. Histopathological changes due to lindane intoxication indicated shrunken and distorted seminiferous tubules, sparse Leydig cells and blood vessels and atrophy in the tissue. The testis weight also decreased significantly. Lindane treated group showed increased lipid peroxidation, whereas glutathione, glutathione peroxidase, superoxide dismutase, catalase and protein were significantly decreased compared to control. Lindane induced damage was minimized by administration of antioxidants. Results suggest that combined pretreatment with antioxidants can alleviate the damage caused to testis by lindane.

Augmentation of cholinesterases and ATPase activities in the cerebellum and pons-medulla oblongata, by a combination of antioxidants (resveratrol, ascorbic acid, alpha-lipoic acid and vitamin E), in acutely lindane intoxicated mice.

In the present investigation neurotoxic effects of lindane and the protective potential of a combination of antioxidants against lindane-induced toxicity were evaluated in Swiss mice. The investigation was carried out on acetylcholinesterase (AChE), butyrylcholinesterase (BChE) and adenosine triphosphatase (ATPase) activities of the cerebellum and pons-medulla oblongata. Healthy mice, 7-8 weeks old were administered acute dose of lindane (40 mg/kg b.w.), antioxidants, both lindane and antioxidants, and vehicle in four separate groups, subcutaneously. Resveratrol (Res), ascorbic acid (C), alpha-lipoic acid (ALA) and vitamin E (E) were used in the combination for neuroprotection at the concentration of 5 mg/kg b.w., 50 mg/kg b.w., 20 mg/kg b.w. and 50 mg/kg b.w. respectively. Enzymatic activities were used as biochemical marker for manifestation of lindane-induced acute toxicity. Protective effects of antioxidants were also evaluated using the same parameters. Treatment of lindane to normal control animals resulted in a significant decrease in AChE, BChE and ATPase levels in crude homogenates of cerebellum and pons-medulla. Antioxidants treatment significantly increased the levels of enzymes. Critical difference (CD) of AChE, BChE and ATPase levels in various groups was found significant at 1% in cerebellum and pons-medulla both (i.e. P<0.01).

Ameliorative effect of a combination of vitamin E, vitamin C, alpha-lipoic acid and stilbene resveratrol on lindane induced toxicity in mice olfactory lobe and cerebrum.

Acute dose of lindane (40 mg/kg body weight, ip) caused significant reduction in butyrylcholinesterase (BChE) activity both in olfactory lobe and cerebrum of mice along with reduction in catalase (CAT), total protein and elevation in superoxide dismutase (SOD) and cholesterol contents. Pretreatment by a combination of antioxidants, vitamin E, vitamin C, a- lipoic acid and stilbene resveratrol (125 mg/kg body weight, ip) significantly augment the altered level of BChE and protect the other parameters in both the brain regions. The results were adequately in agreement with the histochemical findings, suggesting the neuroprotective efficacy of combination of antioxidants studied on the lindane induced neurotoxicity.

The evaluation of effect of alpha-lipoic acid and vitamin E on the lipid peroxidation, gamma-amino butyric acid and serotonin level in the brain of mice (Mus musculus) acutely intoxicated with lindane.

The objective of the present study was to evaluate the neurotoxic effects of lindane, in mice and the protective potential of two antioxidants alpha-lipoic acid (ALA) and vitamin E, against the observed lindane induced toxicity. 7-8 weeks old healthy Swiss mice were administered acute doses of lindane (40 mg/kg b.w.) or antioxidants or both subcutaneously and analyzed 18 h later. ALA and vitamin E were used in the combination for neuroprotection in the concentration of 20 mg/kg b.w. and 50 mg/kg b.w. respectively. Lipid peroxidation, gamma-amino butyric acid (GABA) and serotonin level were used as biochemical test of toxic action for lindane induced acute toxicity. Protective effects of ALA and vitamin E were also evaluated on the same parameters. Reduced glutathione (GSH) and thiobarbituric acid reactive substances (TBARS) level served as an index for determining the extent of lipid peroxidation. Treatment of lindane to normal control animals resulted in a significant decrease and increase in GSH (P<0.01) and TBARS level (P<0.01) respectively in crude homogenate of whole brain. Antioxidants treatment significantly altered the level of GSH (P<0.01) and TBARS (P<0.01). GABA and serotonin level in whole brain as well as in different regions of brain were measured. Main brain regions under the investigation were olfactory lobe, cerebrum, hippocampus-hypothalamus, cerebellum and pons-medulla. Critical difference (CD) of GABA level in various groups was found significant at 1% in cerebrum and hippocampus-hypothalamus, at 5% in whole brain, cerebellum and pons-medulla (i.e. P<0.01 and P<0.05 respectively). Change in serotonin level in whole brain as well as in all studied brain regions of various groups was found significant at 1% CD (i.e. P<0.01).

Modulation of tricarboxylic acid cycle dehydrogenases during hepatocarcinogenesis induced by hexachlorocyclohexane in mice.

The sequential distribution of key tricarboxylic acid (TCA) cycle enzymes have been investigated during hexachlorocyclohexane (HCH)-induced hepatocarcinogenesis in Swiss mice. Animals were continuously exposed to HCH (500ppm) for 2, 4, and 6 months until liver tumor developed. The activity of TCA cycle enzymes such as isocitrate dehydrogenase (ICDH), succinate dehydrogenase (SDH), and malate dehydrogenase (MDH) have been studied. The activity of all the enzymes declined after 2 months of exposure of HCH in the liver. The neoplastic nodules and tumors developed after an exposure of HCH for 4 and 6 months, respectively. Neoplastic nodule and tumor showed wide variations in the activity and distribution of TCA cycle enzymes. The decreasing pattern in the activity of enzymes persisted in the non-neoplastic and non-tumor regions of the liver except SDH. However, the cells in nodular area and tumor showed intense enzymatic activities at cellular level. In the nodular region SDH activity declined prominently, whereas the non-nodular area showed positive reaction. Conspicuously, the tumor showed islands of positive and negative zones for TCA cycle dehydrogenases. The significance and relevance of such a distribution pattern still remains a mystery. The results are discussed in the light of HCH-induced toxicity on energy metabolism in exposed animals and possible role of such enzymes in the tumor formation.