Amino Acid Transport System of the Guinea Pig Small Intestine is Injured by Hydroxyl Radicals

Abstract

The mechanism for the damage to the alanine-preferring amino acid transport system (A system) of guinea pig intestinal brush border membrane vesicles induced by active oxygen species was studied in vitro. The transport activity of L-proline, which is a model amino acid for the A system, and the tryptophan fluorescence intensity of intestinal brush border membrane vesicles were decreased, and lipid peroxidation of these membrane vesicles was induced by ultraviolet irradiation, which generated active oxygen species. Thiourea (hydroxyl radical scavenger) protected L-proline transport activity and tryptophan fluorescence intensity of intestinal brush border membrane vesicles and also inhibited lipid peroxidation in these membrane vesicles in the presence of active oxygen radicals. a-Tocopherol (singlet oxygen radical scavenger) inhibited lipid peroxidation of intestinal brush border membrane vesicles but protected neither L-proline transport activity nor trytophan fluorescence intensity in these membrane vesicles in the presence of active oxygen radicals. Catalase and superoxide dismutase showed no protective effect on L-proline transport activity, tryptophan fluorescence intensity, or lipid peroxide formation in intestinal brush border membrane vesicles in the presence of active oxygen radicals. These results suggest that the hydroxyl radicals play an important role in the damage to intestinal amino acid transport activity induced by active oxygen species and that this damage induced by hydroxyl radicals can be attributed to lipid peroxidation and decomposition of aromatic amino acids of membrane protein in intestinal brush border membrane vesicles.

Key Words:

• Amino acid
• hydroxyl radical
• intestine
• lipid peroxidation
• ransport
• tryptophan residue