Relative bioavailability of two brands of ornidazole in twelve healthy volunteers.

AIM OF THE STUDY: To determine the bioequivalence of two marketed ornidazole formulations in healthy volunteers. METHODOLOGY: A single dose relative bioavailability of Ornidazole 1.5 g (3 x 500 mg tablets) of test product (Giro, Panacea Biotec Ltd.) and that of standard reference (Dazolic, Sun Pharmaceutical Industries), was investigated in healthy adult males. A total of 12 subjects wee enrolled in the study and investigations consisted of two treatment phases separated by a washout period of seven days. Both treatment phases were of 12 hours durations each. Blood samples were collected at 0, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 10 and 12 hours post-administration of assigned drug product. Appropriate fasting restrictions were employed during both the treatment phases. Drug assay was done using HPTLC method. The statistical significance of difference in pharmacokinetic parameters between preparations was tested using ANOVA. RESULTS: The mean peak plasma concentration (Cmax) of 32.67 +/- 4.45 microg/ml was achieved at 1.54 +/- 0.81 hours following administration of test product as against mean Cmax of 31.55 +/- 5.04 microg/ml at 1.79 +/- 0.89 hours for reference standard. The area under time concentration curve (AUC(0-12)) hours was 261.67 +/- 77 microg/ml hours with reference standard and 265.41 +/- 30.82 microg/ml hours for test product. CONCLUSION: There was no statistically significant difference between the two formulations and the two products

Comparative bioavailability study of clonazepam after oral administration of two tablet formulations.

OBJECTIVE: To assess the bioavailability of clonazepam from two brands of 2 mg tablet formulations--Epitril and reference brand. METHODS: A two-way randomised cross-over bioavailability study was carried out in 12 healthy male volunteers. Coded plasma samples were analysed for levels of clonazepam by high performance liquid chromatography (HPLC) method. RESULTS: The mean Cmax, Tmax t1/2 beta and AUC (0-48) for Epitril were: 16.31 +/- 3.07 ng/mL, 1.63 +/- 0.48 h, 46.97 +/- 12.26 h and 207.70 +/- 57.07 ng/ml.h; for reference brand were 19.75 +/- 5.95 ng/mL, 1.42 +/- 0.29 h, 46.88 +/- 11.29 h and 215.70 +/- 50.89 ng/ml.h respectively. These were comparable and the differences were not statistically significant. CONCLUSION: Based on above pharmacokinetic parameters, Epitril was bioequivalent to reference brand.

Effect of D-400, a herbal formulation, on blood sugar of normal and alloxan-induced diabetic rats.

Blood sugar levels of normal rats treated with D-400 showed significant reduction (P < 0.05) as compared to control groups. The fall was seen at one month and remained so uptill 3 months. Hyperglycemic response to adrenaline was significantly lowered (P < 0.05) following D-400 treatment. D-400 potentiated the hypoglycemia following tolbutamide treatment. Blood sugar remained persistently low in tolbutamide plus D-400 treated group after 3 and 4 hours (P < 0.05). In the alloxan-induced diabetic rats, a significant lowering of blood and urinary sugar was noticed on day 20, 30 and 40 following treatment with D-400 (P < 0.05). Liver glycogen depletion was significantly inhibited in the D-400 treated group (P < 0.025). D-400 has significantly potentiated (P < 0.05) the hypoglycemic action of insulin in alloxan-induced diabetic rats.

Immunotherapeutic modification by an ayurvedic formulation Septilin.

Effect of Septilin, an ayurvedic formulation proven to be effective in the therapy of chronic infections, was investigated on the phagocytic system and humoral response in rats and mice. Septilin exhibited significant protection in E. coli-induced abdominal sepsis in normal mice and in Staphylococcus aureus-induced sepsis in neutropenic mice. It significantly reduced the viable E. coli cells when incubated with neutrophils in rats. Septilin stimulated the phagocytic function of the reticuloendothelial system in mice. In normal rats, Septilin enhanced anti-SRBC hemagglutination antibody titre by 5.7-fold and showed significant protection in cyclophosphamide-induced humoral suppression.

Protective effect of Liv.52 on alcohol-induced fetotoxicity.

The adverse effects of maternal alcohol consumption on the development of the fetus are well known. The adverse effects of ethanol on the liver are now believed to be due to acetaldehyde formed as an intermediate metabolite of ethanol. Liv.52 has been shown to bring about faster elimination of acetaldehyde from the body and thus prevent alcoholic liver damage. Other toxic effects of alcohol may also be due to acetaldehyde and may be prevented by Liv.52. In this study, rats were given 20% (v/v) ethanol in drinking water, during the gestation period, and the effect on maternal body weight and fetal outcome was noted. The protective effect of Liv.52 administration during the gestation period was studied. The results show that ethanol ingestion caused a decrease in gestational weight gain, total fetal weight, and number of live fetuses. There were increases in resorptions. Liv.52 administration reduced the deleterious effects of ethanol. The concentration of acetaldehyde in the amniotic fluid of ethanol-consuming animals was 0.727 microgram/ml. Liv.52 administration lowered it to 0.244 microgram/ml. The protective effect of Liv.52 could be due to the rapid elimination of acetaldehyde.

Alcohol hangover and Liv.52.

Ethanol and acetaldehyde levels in blood and urine have been evaluated in 9 volunteers following administration of Liv.52 and placebo on the evening of the study and on the following morning. On the following morning the volunteers scored their symptoms and completed visual analogue scales. Single dose and multiple dose studies were done. Liv.52 produced a considerable reduction in blood and urine levels of ethanol and acetaldehyde after 12 h. It is possible that Liv.52 prevents the binding of acetaldehyde, bringing about higher initial blood levels followed by rapid elimination. It reduced the hangover symptoms.

Effect of Liv.52, a herbal preparation, on absorption and metabolism of ethanol in humans.

In 8 social drinkers, the effect of a single dose of Liv.52 or placebo on ethanol absorption has been studied after ingestion of 30 ml whisky in 5 min. The t1/2 absorption with Liv.52 was 3.62 min, significantly less than after placebo, 6.29 min. The peak concentration after Liv.52 (49.9 mg.100 ml-1) was significantly higher than with placebo (40.5 mg.100 ml-1). Whisky 120 ml consumed by regular alcohol users in 1 h, before and following 15 days of Liv.52 treatment produced significantly higher ethanol levels at 2, 3 and 4 h and significantly lower acetaldehyde levels at 3 and 4 h after Liv.52 treatment. Liv.52 enhanced the rate of absorption of ethanol and rapidly reduced acetaldehyde levels, which may explain its hepatoprotective effect on ethanol-induced liver damage.