The purpose of this study was to determine the effects of dietary fat, vitamin E and iron on oxidative damage and antioxidant status. Male Swiss-Webster mice (1 mo old) were fed a basal vitamin E-deficient diet that contained either 8% fish oil + 2% corn oil or 10% lard with or without 1 g dl-alpha-tocopheryl acetate. The diets without vitamin E contained either 0.21 or 0.95 g ferric citrate/kg. Diets were fed for 4 wk/kg diet. Compared with the vitamin E-supplemented groups, mice fed diets without vitamin E (with or without supplemental iron) had significantly (P < 0.05) higher hepatic levels of thiobarbituric acid-reactive substances (TBARS), conjugated dienes and protein carbonyls when they were fed fish oil, but not lard. The levels of TBARS were further increased by iron supplementation in the mice fed fish oil. Significantly lower concentrations of alpha-tocopherol and higher glutathione (GSH) were found in the liver of mice fed fish oil and vitamin E than in those fed lard and vitamin E (P < 0.05). The activities of superoxide dismutase and glucose-6-phosphate dehydrogenase were lower in the fish oil-fed mice than in those fed lard (P < 0.05). The activities of Se-GSH peroxidase, non-Se-GSH peroxidase, catalase, and glutathione reductase were not altered by dietary fat or vitamin E/iron. The results obtained provide experimental evidence of the prooxidative effects of high dietary fish oil and iron, and suggest that vitamin E protects not only lipid-soluble compounds, but also water-soluble constituents, against oxidative damage. Further, dietary lipid plays a key role in determining cellular susceptibility to oxidative stress.

Iodine deficiency with high prevalence of goitre was recognized among pregnant women in an area that previously appeared to be iodine sufficient. An unexpected mild iodine deficiency was also noted in the non-pregnant control group. Reassessment and continuous monitoring of iodine nutritional status is warranted even in populations that are apparently considered to be 'at no risk' of iodine deficiency, especially in pregnant women. Regular administration of iodine, starting at preconception or in early pregnancy and continuing during the period of nursing, is recommended in these regions.

Cats can lose 25 to 30% of their obese body weight over 7 to 9 weeks without developing overt clinical signs of HL, provided that weight-reduction diets are highly palatable, contain a high quality protein, have a source of LCEFA, and are fortified with vitamins and microminerals. However, rapid weight loss may increase risk factors associated with development of diabetes mellitus.

These data provide direct evidence that dietary protein quality alters fatty acid composition of tissues during weight loss in cats. The fatty acid patterns observed suggest that protein quality may alter fatty acid composition through modulation of desaturase activity.

In cats undergoing rapid weight loss there is neither increased triglyceride synthesis nor decreased transport of very low density lipoproteins from the liver, suggesting that their involvement in the development of hepatic lipidosis may be minimal.