Administration of pentazocine to adult male rats (3mg/kg body weight/day) for 10 or 20 days decreased their body weight significantly. The protein content of the serum also decreased significantly, whereas glucose level was elevated significantly only in the 20-day treatment group. Serum enzymes SGOT and SGPT exhibited increased activity after 10 or 20 days of administration of pentazocine, whereas the nonspecific serum esterases showed reduced activity. Further, the results showed the administration of pentazocine increased the serum total lipids, cholesterol, triglycerides, and phospholipids. The data suggest that the administration of pentazocine interferes with lipid metabolism and that it may alter metabolic function. Thus, the present study demonstrates that the administration of pentazocine modifies the biochemical contents and enzymes and thereby is likely to affect the structure and function of vital metabolic organs.
Oral administration of Picrorrhiza kurroa extract was found to reduce the hepatotoxicity and fibrosis induced by chronic administration of carbon tetrachloride and thioacetamide in rats significantly. This was evident from the decreased values of serum and liver lipid peroxides, alkaline phosphatase, and glutamate pyruvate transaminase. Moreover, elevated liver collagen hydroxyproline, which is a marker of fibrosis, was found to be decreased significantly by the oral administration of the P. kurroa extract. P. kurroa was found to be a potent inhibitor of lipid peroxide formation and to scavenge hydroxyl and superoxide radicals in vitro, and this free radical scavenging activity was implicated in the action of the extract. The results are indicative of the usefulness of the P. kurroa extract in conditions of liver fibrosis produced by various xenobiotic agents.
Changes in the activities of lysosomal enzymes (β-D-galactosidase, β-D-glucosidase, β-D-N-acetyl glucosaminidase, and β-fucosidase), mitochondrial enzymes (isocitrate dehydrogenase, malate dehydrogenase, succinate dehydrogenase, α-ketoglutarate dehydrogenase, and NADH dehydrogenase) and marker enzymes of cardiac function (LDH, AST, ALT, and CK) during isoproterenol-induced myocardial infarction and the effect of L-arginine pre-treatment were studied in male albino rats. In the rats given isoproterenol, there were significant increases in serum activities of LDH, CK, AST, and ALT and significant reductions in the myocardial tissue. Activity of the lysosomal enzyme β-D-N-acetyl glucosaminidase was considerably increased, and β-galactosidase was considerably decreased in the isoproterenol-treated rats as compared with that in those given isoproterenol after pre-treatment with L-arginine. The activities of the mitochondrial enzymes in the isoproterenol-intoxicated group were significantly lower as compared with those of the L-arginine supplemented rats given isoproterenol. These results confirm the efficacy of L-arginine as a potent cardioprotective agent and the protective effect of L-arginine against isoproterenol-induced mitochondrial and lysosomal damage.
Alteration of serum electrolytes (Na+, K+, Cl-, and HCO3-) was studied in Zebu cattle experimentally infected with 11.0×106Trypanosoma vivax. Another group of similarly infected cattle was intravenously infused with lactose in normal saline, at a dose rate of 0.5g/kg body weight as a function of the animal blood volumes of about 6-7% their body weights. Serum Na+ and Cl- concentrations showed significant (p<0.05) increases following decreasing parasitemia on days 6, 7, and 8 post infection (p.i.), whereas the greatest drops, resulting in hyponatremia and hypochloremia, occurred at the period when parasites were very scant in the blood. The Na+ and Cl- returned to normalcy between days 10 and 13p.i., coinciding with the second parasitemic wave. K+ values showed a nonsignificant decline following the decline of parasitemia, and rose to normal values thereafter, around the second wave of parasitemia. The HCO3- values were lowest when the parasites became numerous in the blood on day 3p.i., with a significant (p<0.05) decrease at peak parasitemia on day 5p.i. Subsequently, HCO3- concentrations increased when parasites became low in number in the peripheral circulation; thereafter, interrupted but significant (p<0.05) increases in HCO3- values occurred as the disease progressed. With the i.v. infusion of lactose in normal saline when the disease had been established, evidenced by peak parasitemia and declining packed cell volume (PCV), serum Na+ and Cl- remained normal as observed in the first uninfected uninfused group. The variations of K+ and HCO3- showed a similar pattern during the infusion. The values of all four electrolytes were relatively reduced immediately after and during the course of the infusion. The anion gaps were 20-22mM/liter for the uninfected group; 22-25mM/liter on days 3-5p.i. and 16-19mM/liter on days 6-13p.i, for the infected, uninfused group. Whereas infusion into the infected group produced an anion gap of 15-25mM/liter. The choice of saline as a solvent for lactose and the total infusion volume had no detrimental effect on the host's electrolytes and acid-base status; rather, the infusion ameliorated the aberrations in electrolytes associated with T. vivax in cattle.
The effects of administration of vitamin E on hyperoxaluria, hypercalciuria, hyperuricosuria, and hypocitraturia and on the decreased levels of antioxidants such as ascorbic acid, vitamin E, glutathione (GSH), and superoxide dismutase (SOD) in kidney stone patients were observed. Following the surgical removal of kidney stones from the patients, vitamin E (200mg/day) was administered from the 7th day onwards to twenty patients for up to 90 days. The normalization process of urinary risk factors and antioxidants was rapid in the vitamin E-administered patients when compared with that in the untreated group. The increased excretion of citrate following vitamin E administration was suggested to reduce the retention of calcium oxalate crystals and thereby lower the rate of recurrence of stones.
The present study was carried out on normal subjects (n=20) and hypertensive patients (n=20) to find the possible difference between the urinary parameters and antioxidant status. We found that hypertensives had hypocitraturia (p<0.001), hypercalciuria (p<0.01), increased lipid peroxide (p<0.001) in plasma, a decreased level of reduced glutathione (p<0.001) and decreased superoxide dismutase activity (p<0.001) in their hemolysate when compared with normals. The altered antioxidant status may cause decreased excretion of citrate and increased excretion of calcium in the urine of hypertensive patients. Hypocitraturia and hypercalciuria were regarded as a pathogenic link between hypertension and renal stone formation.