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Biomedical subjects

I R Rowland

Publications and source records attributed to I R Rowland.

At least 109 records · Page 6Linked to original sources
PubMed1983

Metabolic profile of caecal micro-organisms from rats fed indigestible plant cell-wall components.

A fibre-free diet, or the same diet supplemented with 100 g cabbage or carrot cell-wall preparation/kg, was fed to rats for 28 days and the activities of a number of caecal microbial enzymes (azoreductase, aryl nitroreductase, beta-glucosidase, beta-glucuronidase, imidazole nitroreductase and nitrite reductase) were determined in vitro. The plant cell-wall preparations diluted the gut contents and decreased the number of bacteria per gram of caecal contents. Enzyme activities per gram of caecal contents were also decreased, with the exception of beta-glucosidase activity which was significantly increased. These plant cell-wall preparations also increased caecal size, and thereby significantly increased total activity per caecum of microbial azoreductase, aryl nitroreductase, beta-glucosidase and beta-glucuronidase. When bacterial metabolism was expressed per 10(9) bacteria, all enzyme activities were significantly increased in caecal samples from rats fed the plant cell-wall preparations. There was an overall concordance of 0.91 between all the enzymes when expressed per 10(9) bacteria, but of only 0.38 when enzyme activities were expressed per gram of caecal contents.

Animals↗
PubMed1983

Dietary protein and cecal microbial metabolism in the rat.

Adult rats were fed diets containing 0, 25, 50, 100, 200, or 400 g lactalbumin/kg diet for 10 days, and the activities of six cecal microbial enzymes were determined. Total activity per cecum of azoreductase, beta-glucosidase, and urease increased significantly with increasing dietary protein, whereas the activities of beta-glucuronidase and nitroreductase were not significantly affected. Nitrate reductase activity decreased significantly. Total numbers of cecal bacteria were not significantly altered by the treatment.

Animals↗
PubMed1983

Interaction between pectin and rat hindgut microflora.

The contents of the lower alimentary tract from rats fed a semisynthetic, pectin-supplemented diet showed increased nitrate reductase activity and an increase in the amount of luminal contents in the intestine and cecum. Nitrate reductase activity was associated with the insoluble fraction of the gut contents which was sedimented by centrifugation (5,100 X g,20 min) and was abolished after treating the animals with streptomycin, neomycin, and bacitracin for 7 days. The pectin-dependent increase in cecal size and microbial nitrate reduction were reversed when animals were transferred from a pectin-supplemented onto a control semisynthetic diet. Polygalacturonic acid (pectic acid) was without effect on either cecal size or cecal microbial nitrate reductase activity. The studies demonstrate that pectin influences microbial metabolism in the alimentary tract.

Animals↗
PubMed1983

Metabolic activity and enzyme induction in rat fecal microflora maintained in continuous culture.

The enzyme activity of the rat hindgut microflora maintained in an anaerobic two-stage continuous culture was compared with that of rat cecal contents. A qualitative comparison (API ZYM) showed a high degree of similarity between the two populations. Quantitative determinations showed that azoreductase, beta-glucosidase, nitrate reductase, and nitroreductase activities were comparable, and that beta-glucuronidase activity was very low in the culture. beta-Glucuronidase, beta-glucosidase, and nitrate reductase activities were induced within the culture by their respective substrates. Bile acids influenced microbial activity in vitro, with cholic acid inducing beta-glucosidase, azoreductase, and beta-glucuronidase activities and decreasing nitrate reductase activity. Chenodeoxycholic acid increased beta-glucosidase and beta-glucuronidase activities and decreased azoreductase, nitrate reductase, and nitroreductase activities in vitro. These studies demonstrate that the rat hindgut microflora may be successfully cultured in vitro and suggest control mechanisms that regulate the metabolic activity of these organisms in vivo.

Animals↗
PubMed1983

Effect of dietary carrageenan and pectin on the reduction of nitro-compounds by the rat caecal microflora.

Rats were fed either a basal purified diet, or that diet supplemented with 50 g/kg pectin or iota carrageenan for 50 days, and caecal microbial nitroreductase activity determined using p-nitrobenzoic acid, p-nitrophenol, 2,4-dinitrotoluene, nitrofurantoin and metronidazole as substrates. Both pectin and carrageenan increased the weight of caecal contents, and pectin also increased the number of bacteria per caecum. In contrast, carrageenan decreased the caecal bacterial population. Pectin significantly increased the rate of reduction of metronidazole and the rate of conversion of p-nitrobenzoic acid to p-aminobenzoic acid, while carrageenan significantly decreased the rate of reduction of every compound studied. The results demonstrate that microbial reduction of the nitro-group may be altered by diet, although the response found with one nitro-compound may differ from that seen with another substrate.

Animals↗
PubMed1982

Reduction and methylation of sodium arsenate in the rat.

After a single oral dose of sodium [74As] arsenate to male Wistar rats, arsenic was rapidly absorbed and accumulated in the blood and to a lesser extent in the liver, kidneys, lungs and spleen. Within 1 h of dosing, arsenic was present in the blood, liver and spleen predominantly in the methylated forms (methylarsonic acid and dimethylarsinic acid), whereas in the lung and kidneys, approximately 50% was in the inorganic form. Intravenous injection of sodium [74As] arsenate resulted in a pattern of arsenic species in the blood and kidneys similar to that seen after oral administration, suggesting that the gut flora does not contribute significantly to biotransformation of arsenic in vivo. Analysis of the forms of arsenic in portal blood after administration of arsenate via the small intestine revealed a rapid reduction of arsenate to arsenite, followed by linear rates of production of methylarsonic acid and dimethylarsinic acid.

Animals↗
PubMed1982

Species differences in the testicular toxicity of phthalate esters.

Oral administration of di-n-butylphthalate (DBP) produced uniformly severe seminiferous tubular atrophy in rats and guinea pigs but caused only focal atrophy in mice. Hamsters showed no testicular changes with DBP and only minor changes in response to di-(2-ethylhexyl)phthalate (DEHP) and di-n-pentylphthalate (DPP). The rate of intestinal monohydrolysis of DEHP was slower in hamsters than in rats and this may be important, as mono-(2-ethylhexyl)phthalate (MEHP) did cause focal seminiferous tubular atrophy in hamsters. However, mono-n-butylphthalate (MBP) had no such effect. The decrease in testicular zinc concentration and enhancement of urinary zinc excretion produced in rats by DEHP and DPP was not observed in hamsters. Thus, species differ widely in their sensitivity to the testicular toxicity of phthalate esters.

Animals↗
PubMed1982

Short-term toxicity study of carnauba was in rats.

Groups of 15 male and 15 female rats were fed diet containing 0 (control), 1, 5 or 10% carnauba wax or 10% cellulose powder for 13 wk and groups of five rats of each sex were given these treatments, except the 1% carnauba wax, for 2 or 6 wk. Rats given 10% carnauba wax or 10% cellulose consumed more food than the controls but showed no differences in body weight, an effect attributed to the dilution of the diet by non-nutrient test materials. The study showed no treatment-related differences in body weights, water intakes, haematological values, serum-enzyme activities, urinary concentration and 'dilution' tests, organ weights or histological findings. The no-untoward-effect level for carnauba wax in the diet was 10%, which represented a mean intake of approximately 8.8 and 10.2 g/kg body weight/day in males and females, respectively.

Animals↗
PubMed1982

Dietary fibre, bacterial metabolism and toxicity of nitrate in the rat.

1. A semi-synthetic diet, the semi-synthetic diet plus pectin, and a stock diet were fed to rats, and three metabolic functions of the caecal bacteria (reduction of amaranth, p-nitrobenzoic acid and nitrate) were measured in vitro. 2. No consistent differences were noted between diets for the reduction of amaranth and p-nitrobenzoic acid. 3. No consistent differences in nitrate reductase activity were noted for rats maintained on a stock diet or a fibre-free diet. However, the addition of 5% pectin to the latter diet resulted in a several-fold increase in nitrite production. 4. This increased nitrite production in vitro was associated with methaemoglobinaemia following the oral administration of nitrate to rats fed the diet containing pectin. Animals receiving the basal fibre-free diet were unaffected by nitrate.

Animals↗
PubMed1981

In vitro metabolism of inorganic arsenic by the gastro-intestinal microflora of the rat.

The contents of the rat small intestine or caecum reduced sodium [74As] arsenate to arsenite over a period of 2-3 days. In the presence of caecal, but not small intestine, contents, small amounts of methyl arsonic acid and dimethylarsinic acid were formed. Stomach contents reduced arsenic very slowly. The metabolism of arsenate was inhibited by autoclaving the gut contents or by adding antibiotics, thus indicating that bacteria were involved. In prereduced media containing thioglycollate or cysteine in the absence of intestinal bacteria, sodium arsenate was reduced to arsenite. The rate of reduction of arsenate by the gut flora was increased by the presence of hydrogen sulphide or bile acids.

Animals↗
PubMed1980

Substrates and inhibitors of hepatic amine oxidase inhibit dimethylnitrosamine-induced mutagenesis in Salmonella typhimurium.

The mutagenic effect of dimethylnitrosamine in Salmonella typhimurium TA100, in the presence of a rat-liver homogenate derived from animals treated with Aroclor 1254, was inhibited by substrates and inhibitors of monoamine oxidase. Substrates of diamine oxidase did not inhibit dimethylnitrosamine mutagenesis and, furthermore, monoamine oxidase inhibitors had no effect on mutagenesis by benzo[a]pyrene or aflatoxin B1. The results suggest that monoamine oxidase participates in the activation of dimethylnitrosamine to a mutagen.

Animals↗
PubMed1978

Metabolism of methylmercuric chloride by the gastro-intestinal flora of the rat.

1. The contents of the caecum and small intestine of the rat metabolized methylmercuric chloride in vitro to a volatile product over a period of 3 to 4 days. The bacterial flora of the gut were responsible for the metabolism. 2. in the presence of caecal contents methylmercury was reduced to metallic mercury. 3. The contents of the small intestine metabolized methylmercuric chloride indirectly, as a result of prior synthesis of H2S to a volatile sulphur derivative of methylmercury.

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