OBJECTIVEIn order to investigate that ascorbic acid deficiency is responsible for lathyrus toxicity, the effect of dietary feeding of lathyrus pulse in normal and scorbutic guinea pigs for 3 months, on intestinal biochemical parameters was undertaken.

METHODSThe intestinal brush border membrane (BBM) marker and xenobiotic metabolising enzymes (XME) were assayed.

RESULTSExposure to 80% lathyrus alone and in scorbutic conditions showed significant inhibition of alkaline phosphatase (28%-30%), sucrase (19%) and gamma-glutamyl transpeptidase (GGT) (15%-27%) enzymes, while Ca(2+)-Mg(2+)-ATPase was significantly inhibited (38%) in scorbutic plus lathyrus treated group. The phase I XME (AHH) remained unchanged while the phase II enzyme glutathione-S-transferase (GST) was significantly decreased (20%-22%) in lathyrus and scorbutic plus lathyrus treated groups. Quinone reductase (QR) activity was found to be significantly decreased in lathyrus exposed group (20%). The intestinal biomarker contents including hexose (25%-34%) and phospholipids (20%-40%) were significantly reduced in lathyrus and scorbutic plus lathyrus exposed animals, while sialic acid showed a significant decrease (28%) in scorbutic plus lathyrus treated group. However, cholesterol levels were significantly enhanced (15%-28%) in lathyrus and scorbutic plus lathyrus treated animals.

CONCLUSIONThe results indicate that oral feeding of lathyrus pulse to guinea pigs can alter BBM parameters as well as XME, which may result in the intestinal toxicity. Further, ascorbic acid deficiency could be one of the pre-disposing factors of lathyrus toxicity.

Administration, Oral ; Animals ; Ascorbic Acid Deficiency ; complications ; veterinary ; Biomarkers ; analysis ; Cholesterol ; blood ; Diet ; Digestive System ; enzymology ; metabolism ; pathology ; Guinea Pigs ; Lathyrus ; chemistry ; Male ; Microvilli ; Phospholipids ; metabolism ; Plant Extracts ; adverse effects

OBJECTIVE3-Bromobenzanthrone (3-BBA), an anthraquinone intermediate dye, is extensively used in textile industry. Since, our prior studies have shown that 3-BBA caused significant depletion of ascorbic acid (AsA) levels, the effect of exogenous supplementation of AsA on the urinary elimination of 3-BBA metabolites was investigated.

METHODGuinea pigs were treated with single oral dose of 3-BBA (50 mg/kg b. wt.) in groundnut oil while another group was treated with single oral dose of 3-BBA (50 mg/kg b. wt.) along with 3 day prior and post oral supplementation of AsA. Control groups were either treated with groundnut oil or AsA alone. Urine from individual animals was collected, extracted and analysed on HPTLC.

RESULTSThe highest elimination of 3-BBA (75 microg) was found to be in 0-24 h urine fraction which decreased to 18 microg and 5 microg in the two subsequent 24 hourly fractions of urine. Exogenous supplementation of AsA increased the total urinary elimination of 3-BBA by almost 77%. A total of 10 fluorescent metabolites excluding the parent compound were eliminated in the urine of guinea pigs treated with 3-BBA. Densitometric scanning of chromatogram showed different peaks at Rf 0.18, 0.22, 0.27, 0.34, 0.40, 0.48, 0.56, 0.66, 0.72, 0.80, and 0.95 which were eliminated and marked as urinary metabolite 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, and 11 respectively. AsA not only significantly enhanced the elimination of 3-BBA metabolites but also modified the pattern of metabolites drastically in 0-6 h, 6-24 h and 24-48 h urine fractions.

CONCLUSIONThese results indicate that AsA may be useful in protecting the toxicity of 3-BBA by fascilitating the urinary metabolite(s) excretion of 3-BBA.

Administration, Oral ; Animals ; Antioxidants ; pharmacology ; Ascorbic Acid ; pharmacology ; urine ; Benz(a)Anthracenes ; analysis ; metabolism ; Chromatography, High Pressure Liquid ; Guinea Pigs ; Lipid Peroxidation ; drug effects ; Plant Oils ; metabolism ; Time Factors

The study was designed to investigate the role of hepatic metabolic activity on body burden of HCH residue. Male albino rats were orally administered 0, 5, and 10 mg/kg HCH for 90 days, followed by either sodium phenobarbital or carbon tetrachloride treatment for 0, 15 and 30 days after withdrawal of their respective HCH administration. The liver weight was significantly increased at 30 days after the administration of phenobarbital and carbon tetrachloride in both 5 mg and 10 mg/kg HCH withdrawal groups when compared to control. HCH residue was maximum in fat followed by adrenal > thymus > liver > kidney > spleen > tests > brain > plasma. Carbon tetrachloride caused an accumulation of HCH residues in the liver 15 and 30 days after administration of both doses of HCH. Phenobarbital did not show significant variation in HCH residues in hepatic tissue. Phenobarbital treatment caused significant induction of hepatic RED, APD, AHH, GST and QR activities. Significant decreases in activities were observed by carbon tetrachloride when compared to animals treated with HCH alone. The overall results clearly suggest the role of P450 protein on the body burden of HCH residues.
Animals ; Carbon Tetrachloride ; toxicity ; Inactivation, Metabolic ; Lindane ; pharmacokinetics ; toxicity ; Liver ; enzymology ; metabolism ; pathology ; Liver Function Tests ; Male ; Organ Size ; drug effects ; Phenobarbital ; toxicity ; Rats ; Tissue Distribution