The objective of the present work was to evaluate the broadest toxic effect of some synthetic additives of colorants and/or flavors on different body organs and metabolic aspects in rats. A number of chemical food color and flavor additives are routinely added during processing to improve the aesthetic appearance of the dietary items. However, many of them are toxic after prolonged use. In this experiment, a total of 100 male albino rats of Spargue Dawley strain were divided into 10 groups: G(1) was fed basal diet and served as control, G(2): basal diet + Brilliant blue (blue dye, No. 2, 124 mg/kg diet), G(3): basal diet + carmoisine (red dye, No. 3, 70 mg/kg diet), G(4): basal diet + tartrazine (yellow dye, FD & C yellow No. 5, 75 mg/kg diet), G(5): basal diet + trans-anethole (4.5 g/kg diet) G(6): basal diet + propylene glycol (0.25 g/kg diet), G(7): basal diet + vanillin(1.25 g/kg diet), G(8): basal diet + Brilliant blue + propylene glycol, G(9): basal diet + carmoisine + trans-anethole, G(10): basal diet + tartrazine + vanillin for 42 successive days. All food colorants mixed with or without flavor additives induced a significant decrease in body weight, hemoglobin concentration and red blood cell count. Also there was a significant decrease in reduced glutathione content; glutathione-S-transferase and superoxide dismutase activities in both blood and liver compared to control group. On the other hand, a significant increase in serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase activities, bilirubin, urea, creatinine, total protein and albumin were observed in all test groups when compared to control group. Finally, it is advisable to limit the uses of these food colorants and/or food flavor additives especially those used by children.

The aim of the present study is to investigate the potential role of L-arginine or L-citrulline in rats fed high-fat and high-cholesterol (HFC) diet. HFC feeding increased significantly serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, urea and all lipid profiles and decreased significantly serum high-density lipoprotein-cholesterol (HDL-c) and non significantly serum nitric oxide levels. L-arginine or L-citrulline administration reversed the increase in serum AST and ALT activities, urea and all lipid profiles. These effects were associated with a concomitant increase in HDL-c and nitric oxide levels. In general, rats fed HFC diet and orally treated with L-arginine or L-citrulline had higher relative percentage of 18:0, 20:0 and 22:6 and lower 16:0 fatty acids than rats fed HFC diet. Light and transmission electron microscopic findings of the thoracic aorta confirmed the biochemical results and demonstrated structural changes in the endothelial cells of the intimal layer, medial smooth muscle cells as well as in the adventitial layer in HFC fed-animals. However, these findings indicate little structural alterations in animals supplemented with L-arginine or L-citrulline along with HFC feeding. In the present study, L-arginine or L-citrulline was effective hypocholesterolemic and hypolipidemic agents in rats.

The study was designed to evaluate the effects of rice bran (RB) or its oil (RBO) on lipid metabolism, hepatic insulin receptor substrate‐1 (IRS‐1) and hepatic expression of 3‐hydroxy‐3‐methylglutaryl‐Co A (HMG‐CoA) reductase in rats fed high‐fructose diet (HFD). Rats were divided into four groups: Group 1, animals received standard diet as control, while groups 2, 3 and 4 were fed on a HFD. Groups 3 and 4 animals fed HFD containing RB (5%) instead of cellulose and RBO (10%) instead of corn oil, respectively for 5 weeks. Fructose feeding to rats caused significant elevations in plasma glucose, serum insulin, and lipid profile, while serum total antioxidant capacity was significantly reduced compared to control. Hepatic concentration of IRS‐1 was decreased while malondialdehyde (MDA) and HMG‐CoA reductase mRNA were elevated compared to control group. Addition of RB or RBO to fructose fed rats alleviated the hazardous effects of fructose. Practical applications Rats fed high‐fructose diet were used as a model of insulin resistance accompanied by deleterious metabolic consequences including hyperinsulinemia, hyperglycemia, glucose intolerance, hypertriglyceridemia and hypertension in rats and these metabolic effects are similar to those observed in human multi‐metabolic syndrome X. Supplementation of rice bran or rice bran oil to fructose‐fed rats improves insulin resistance and reduces lipo‐ and glucotoxicity.

The aim of this study was to investigate the consequences of exposure to three levels of boric acid (BA) on male rats reproduction, fertility and progeny outcome, with emphasis on testicular DNA level and quality. Adult male rats (12 weeks old) were treated orally with 125, 250 and 500 mg/kg bwt/d of BA for 60 d. The results indicated that BA administration at 125 mg/kg bwt had no adverse effects on fertility, sperm characteristics or prenatal development of the impregnated females. However, at dose 250 mg, BA treatment significantly increased serum nitric oxide, testosterone, estradiol levels and testicular boron and calcium levels and also significantly reduced serum arginase activity, sperm quality and testicular DNA content with minor DNA fragmentation. The impact of BA exposure at dose 250 mg on male rats fertility was translated into increases in pre-implantation loss with a resulting decrease in the number of live fetuses/litter. In addition to the significant alteration of biochemical measurements, observed at dose 250 mg, administration of BA at 500 mg caused testicular atrophy, severe damage of spermatogenesis, spermiation failure and significant reduction of Mg and Zn testicular levels. None of the male rats, treated with 500 mg/kg bwt, could impregnate untreated females, suggesting the occurrence of definitive loss of fertility. In conclusion, BA impaired fertility, in a dose-dependant manner, by targeting the highly proliferative cells, the germ cells, through decreasing DNA synthetic rate rather than the induction of DNA damage.