ABSTRACT
Candida albicans translocation was determined in rats receiving a normal or vitamin E-supplemented and deficient diet submitted to mesenteric ischemia and reperfusion (MIR). The antioxidant effect of vitamin E on lipid peroxidation was also assessed. The animals were divided into six groups submitted to different diets for 30 d. Groups N, NI, NC and NIC were submitted to a normal diet and used as controls, and groups VITE and DEFE received a vitamin E-supplemented and vitamin E-deficient diet, respectively. Groups NIC, VITE and DEFE were submitted to MIR, inoculated with Candida albicans and sacrificed 24 h after the surgical procedure. The antioxidant effect of vitamin E was determined in the liver and gut mucosa using the TBARS method. Candida albicans translocation was assessed in lymph node, liver and kidney specimens. The results showed that lipid peroxidation was lower (p < 0.05) in the vitamin E-supplemented group. However, vitamin E supplementation did not protect the rats against Candida albicans translocation (the translocation in the Group VITE was 100% for lymph nodes).
Subject(s)
Antioxidants/pharmacology , Candida albicans/physiology , Candidiasis/microbiology , Intestinal Mucosa/metabolism , Reperfusion Injury/prevention & control , Vitamin E/pharmacology , Animals , Antioxidants/administration & dosage , Candidiasis/metabolism , Chromatography, High Pressure Liquid/veterinary , Colony Count, Microbial , Intestinal Mucosa/microbiology , Kidney/microbiology , Lipid Peroxidation/drug effects , Liver/microbiology , Lymph Nodes/microbiology , Male , Mesentery , Rats , Rats, Wistar , Reperfusion Injury/metabolism , Thiobarbituric Acid Reactive Substances/analysis , Vitamin E/administration & dosage , Vitamin E/bloodABSTRACT
The regulation of normal oxidative balance include the maintenance of adequate levels of dietary antioxidants such as vitamin E. The objective of this investigation was to study the effect of three different dietary levels of vitamin E (normal, supplemented 20 times higher and deficient) on plasma and liver lipid peroxidation, assayed by determination of thiobarbituric acid reactive substances (TBARS) and vitamin E in plasma and liver and hepatic reduced glutathione. Administration of dietary vitamin E caused a dose-dependent increase in liver and plasma concentration of this vitamin to 42.11 micrograms/g liver and 29.52 mumol/l respectively, in the supplemented group, and a low concentration of TBARS, 0.67 nmol/mg protein, in liver. The group receiving the diet without vitamin E showed high values of hepatic TBARS, 2.95 nmol/mg protein, and low values of reduced glutathione and reduced concentration of hepatic and plasma vitamin E (1.75 micrograms/g liver and 3.67 mumol/l, respectively). In conclusion, the vitamin E deficiency alone induces the liver lipid peroxidation in rats, and maintenance of adequate or higher vitamin E levels acts as a protective factor against free radical generation.
