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Indirect evidence has suggested that lipid peroxidation is associated with iron overload in vivo. As a measure of lipid peroxidation, pentane expired in the breath of rats loaded with an accumulated dose of either 100 mg or 186-200 mg of iron injected intraperitoneally as iron dextran was measured over a 7 to 8 week period, and the effect on pentane production of feeding antioxidant-supplemented diets was determined. By the seventh week of feeding the diets, rats fed 0.3% L-ascorbic acid produced 17% less (P = 0.03) pentane than did rats fed the basal antioxidant-deficient diet, whereas rats fed 0.004% dl-alpha-tocopherol acetate produced 92% less (P less than 0.001). After being fed the basal diet for 7 weeks, iron-loaded rats produced 76 +/- 9 pmol pentane/100 g body wt/min. When synthetic antioxidants were added to the diet at a concentration of 0.25%, the order of effectiveness in decreasing pentane production after 1 week was: N,N'-diphenyl-p-phenylenediamine greater than ethoxyquin greater than butylated hydroxyanisole greater than butylated hydroxytoluene greater than propyl gallate approximately equal to no antioxidant. After removal of either ethoxyquin or N,N'-diphenyl-p-phenylenediamine from the diets for 1 week, pentane production increased to a high level. The total amount of lipid soluble fluorophores in individual spleens of rats fed N,N'-diphenyl-p-phenylenediamine, ethoxyquin, dl-alpha- tocopherol acetate, ascorbic acid and no antioxidant were correlated significantly with the corresponding total integrated amount of pentane produced by the individual rats over the 7 to 8 week period. This study has provided some of the most direct evidence to date that lipid peroxidation is associated with iron overload in vivo.

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The effect of a single dose of ethanol on lipid peroxidation in three groups of rats fed different amounts of vitamin E was determined by the measurement of pentane in the breath. All rats had increased pentane production above basal levels by 15 min following oral administration of 6 g ethanol/kg body wt. The increase in total pentane production during a 13-hr test period after intragastric administration of ethanol was greater in the rats fed the vitamin E-deficient diet than in the rats fed vitamin E-supplemented diets (alpha = 2P = 0.02). The results support the hypothesis that acute ethanol toxicity involves lipid peroxidation and further demonstrate the usefulness in toxicological studies of monitoring pentane as an index of lipid peroxidation in vivo.

The hypothesis that pentane is an in vivo product of lipid peroxidation was confirmed by a study of the effects of a nonbiological antioxidant on pentane production in rats fed a diet deficient in vitamin E and supplemented with 0.0/% N,N'-diphenyl-p-phenylenediamine (DPPD). Seven rats were fed a vitamin E-deficient diet starting at 3 wk of age. After 5 wk, 0.01% DPPD was added to the diets of three rats (group DPPD) while the diet of the other four rats remained unchanged (group OE). Within 2 wk of the diet change, rats in group DPPD exhaled 65% less pentane than rats of the same age in group OE. After 5 wk of being fed the DPPD-supplemented diet, rats in group DPPD were again fed the basal vitamin E-deficient diet; within 3 wk, these rats produced pentane levels similar to those of rats in group OE. The effects of vitamin E depletion and repletion on in vivo lipid peroxidation in rats were also studied. Three groups of three rats each were initially led a vitamin E-deficient diet starting at 3 wk of age. After 8, 8, and 5 wk of being fed this diet, the three groups were led diets supplemented with 3.3 (group 0--~3.3E), 11 (group 0--,11E), and 200 (group 200E) i.u. vitamin E acetate]kg diet, respectively. Another group of three rats (group 11 E) was fed a diet supplemented with 11 i.u. vitamin E/kg starting at 3 wk of age for the duration of the study. There were significant decreases in pentane production by rat groups 0-*3.3E, 0-*11E, and 200E within 2 wk of the change to the vitamin E-supplemented diets. After about 5 wk of being fed their respective vitamin E-supplemented diets, pentane breath levels had stabilized. Breath pentane levels were inversely proportional to the log of dietary vitamin E concentration.

Weanling rats were fed one of 3 diets containing 0, 11 or 200 international units (IU) dl-alpha-tocopherol acetate/kg diet for 4 weeks. Following this period, the drinking water was replaced with an 18% solution of ethanol (v/v). An isocaloric D-glucose solution was substituted for the drinking water of a control group of rats fed the vitamin-E-deficient diet for 4 weeks. The 4 treatment groups were maintained on the diet and drinking regimen for 20 weeks. Basal levels of expired pentane were determined at weeks 0, 1, 3, 5, 7 and 9. Chronic ethanol consumption did not influence basal pentane production during the 9-week treatment. Basal levels of expired pentane were affected by dietary vitamin E. Rats supplemented with vitamin E had basal pentane levels less than one-half of the level of rats fed a vitamin-E-deficient diet (p less than 0.001). After 14 weeks of treatment, the 2 groups of rats fed a vitamin-E-deficient diet were administrated p.o. an acute dose of 6 g of ethanol/kg body wt. Pentane expired above basal levels during the following 4-hr period correlated with the amount of hepatic triglycerides determined at the conclusion of the experiment. The etiology of ethanol toxicity is a complex and multifactorial system made up of many biological variables that influence lipid peroxidation. The appropriate choices of experimental designs and methods are important in examining the role of lipid peroxidation.

The ADPglucose pyrophosphorylases from Rhodopseudomonas sphaeroides and Rhodopseudomonas gelatinosa are activated by fructose-6-phosphate, pyruvate and fructose-1,6 biophosphate-P2. The effects of the activators are to increase significantly the Vmax of ADPglucose synthesis and to lower the S0.5 values (concentration of substrates giving 50% maximal velocity) for ATP and MgCl2. The R. sphaeroides enzyme is inhibited by Pi while the R. gelatinosa enzyme is inhibited by AMP as well as by Pi. The interaction between inhibitor and activator is complex. At very low concentrations of activator the enzyme is more sensitized to inhibition. However, at higher concentrations of activator there is a decrease in the sensitivity of the enzyme towards inhibition. The findings are discussed with respect to glycogen synthesis in these microorganisms and may be related to findings that indicate that Rhodopseudomonads have the ability to degrade sugars via the Entner-Duodoroff or Embden-Meyerhoff pathways.