Robert L. Anderson

The catabolism of the geometric isomers of uniformly 14C-labeled δ9-octadecenoic acid and uniformly 14C-labeled δ9,12-octadecadienoic acid by the fasting rat

Abstract The catabolic fates of the geometric isomers of uniformly 14C-labeled Δ9-octadecenoic acid and uniformly 14C-labeled Δ9,12-octadecadienoic acid were studied in fasting rats. All of the fatty acids were well absorbed (94–97%) regardless of double bond geometry. The cis isomer of [14C]Δ9-octadecenoic acid was catabolized to CO2 to a slightly greater extent (70%) than was the trans-isomer (65%). The extent to which these acids were catabolized by the animal was independent of their level in the diet over a wide range. Catabolism of the trans isomers of [ 14 C ]Δ 9,12 - octadecadienoic acid to CO2 was somewhat greater (68–70%) than that of the all cis isomer (64%). Although there were small differences among the fatty acid isomers with regard to oxidation to CO2, all of the acids were readily oxidized by the rat regardless of their geometric configuration.

Oxidation of the geometric isomers of δ9,12-octadecadienoic acid by rat liver mitochondria

Abstract The comparative catabolism of the geometric isomers of uniformly 14 C-labeled Δ 9,12 -octadecadienoic acid (18:2) by rat liver mitochondria has been investigated. All of the isomers were catabolized to CO 2 , acetoacetic acid, β-hydroxybutyric acid, and the polycarboxylic acids of the citric acid cycle. It is, therefore, concluded that all of these acids are oxidized via the β-oxidation sequence. It was further established that each of the isomers was completely oxidized by the mitochondria with no accumulation of shorter-chain length unsaturated acids. In all incubations the 18:2 isomers containing 1 or 2 trans double bonds were oxidized to a greater extent than the all- cis isomer. The significance and possible cause(s) for this effect of double bond conformation is discussed in light of the substrate specificities of the enzymes of the β-oxidation sequence.

High dose sodium toxicity

The published reports demonstrate effects of high salt intake ranging from direct cellular toxicity to carcinogenicity and increased tumor formation when exposure is concurrent with or following exposure to a variety of carcinogens. Although these responses have been reported for a variety of sodium salts and its is clear that the anionic species often contribute

Trypsin inhibitor ingestion‐induced urinary indican excretion and pancreatic acinar cell hypertrophy

Sodium saccharin (NaSacc) has been shown to be a protease inhibitor and to induce an increase in urinary indican, which is a product that is dependent on microbial metabolism of tryptophan. These findings suggest that urinary indican might provide a noninvasive marker of increased pancreatic acinar cell size associated with plant trypsin inhibitor ingestion. The results demonstrate the 7.5% of dietary NaSacc, which increases urinary indican, also increases relative pancreas mass (g/kg body weight), and that these effects are not induced by intravenous infusion of NaSacc. Dietary soybean trypsin inhibitor in the dose range of 17-713 mg/100 g diet was associated with parallel dose-dependent increases in urinary indican and pancreatic acinar cell size (assessed histologically). These findings suggest that measurement of relative urinary indican excretion (microgram/g diet ingested) can provide a noninvasive marker of increased pancreatic acinar cell size in rats that ingest compounds which inhibit digestive proteases.

Intestinal responses in the male rat to gavaged corn oil.

Gavaged corn oil is readily hydrolyzed and taken up by the rat small intestine but resynthesis to triglyceride and transport are slow. Multiple doses of corn oil caused increases in the non-lipid dry mass, protein and DNA content of the luminal surface of the small intestine. The possible relationship of these effects of gavaged corn oil to pancreatic acinar cell neoplasias is discussed. The fact that corn oil dosed by gavage causes changes in the composition of the small intestinal surface argues against the use of this technique in the assessment of the toxicological characteristics of compounds.

Urinary and bladder responses to immobilization in male rats

Immobilization of groups of five to nine male rats for 2-5 days results in a 50% increase in urinary bladder fresh weight compared with normally caged controls. The increase in urinary bladder weight was not due to tissue oedema and was accompanied by epithelial hyperplasia in some urinary bladders. Immobilization did not alter total urine volume, but it did decrease the frequency of urine voiding and doubled the mean urine weight/voiding. Thus, bladder distention caused by the increased volume per voiding caused a rapidly induced increase in bladder tissue growth, and was accompanied by an increase in bladder epithelial cell division.