Effects of dietary carnosine and vitamin E on antioxidant and oxidative status of rats.

The purpose of this study was to determine if moderate levels of carnosine supplement, alone or in combination with vitamin E, enhance antioxidant status and/or provide protection against oxidative stress. Fifty-four one-month-old male Sprague-Dawley rats were fed a basal vitamin E-deficient diet supplemented with either 0, 200, or 1000 mg L-carnosine, and either 0, 10, or 100 IU vitamin E (as all rec-alpha-tocopheryl acetate) per kg diet for 15 weeks. The antioxidant and oxidative status were assessed in the skeletal muscle, liver, and blood.

Dietary vitamin E reduces labile iron in rat tissues.

Previous studies have shown that dietary vitamin E reduced generation and/or levels of superoxide. As superoxide has potential to release iron from its transport and storage proteins, and labile or available form of iron is capable of catalyzing the formation of reactive hydroxyl radicals, the effect of dietary vitamin E on labile iron pool was studied in rats. One-month-old Sprague-Dawley male and female rats were fed a basal vitamin E-deficient diet supplemented with 0, 20, 200, or 2,000 IU vitamin E/kg diet for 90 days.

Biological functions and metabolic fate of vitamin E revisited.

Information accumulated lately has confirmed the essentiality of vitamin E for humans and provided a better understanding of its biological function and metabolic fate. The discovery of alpha-tocopherol transfer protein, which preferentially binds to RRR-alpha-tocopherol, not only provides conclusive evidence of the essentiality of vitamin E for humans, but also sheds light on the superiority of RRR-alpha-tocopherol biologically over other isomers. The presence of tocopherol regeneration systems and multiple interdependent antioxidant systems is largely responsible for the lack of a widespread deficiency in humans and the difficulty to deplete vitamin E in the adult.

Copper toxicity, oxidative stress, and antioxidant nutrients.

Copper (Cu) is an integral part of many important enzymes involved in a number of vital biological processes. Although normally bound to proteins, Cu may be released and become free to catalyze the formation of highly reactive hydroxyl radicals. Data obtained from in vitro and cell culture studies are largely supportive of Cu's capacity to initiate oxidative damage and interfere with important cellular events.