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지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 저자정보
초록·키워드
The antioxidant activities of carnosine and related compounds (CRCs) including anserine and homocarnosine have been reported mainly using phosphatidylcholine (PC) liposomes. In this study, the antioxidant activities of these compounds and their components, L-histidine and β-alanine were compared using several different in vitro model systems. In either Cu (Ⅱ) or Fe (Ⅲ) + ascorbic acid (AA)-catalyzed deoxyribose system, carnosine, homocarnosine, anserine, and histidine showed a strong inhibitory effect on deoxyribose degradation, as measured by thiobarbituric acid-reactive substances for OH scavenging activity. The inhibitory effect of carnosine, homocarnosine, and anserine was greater in the Cu (Ⅱ) system than the Fe (Ⅲ) system. Although carnosine and anserine stimulated H202 formation in the presence of 10 mM glucose and 10 m M Cu (Ⅱ), they simultaneously inhibited deoxyribose degradation. Histidine-containing dipeptides were very effective for inhibition of lipid peroxidation in PC liposomes, as measured by malondialdehyde, lipid peroxide, and conjugated diene. Among the measurements, there was a correlationship as expected. Carnosine reduced Cu (Ⅱ) to Cu (Ⅰ) and the reducing potential of carnosine was 1/10 of that of AA. CRCs strongly inhibited HOCl-induced AA oxidation but only carnosine and anserine inhibited HOCl-induced inactivation of a-antitrypsin activity in a preincubation time-dependent manner. Carnosine, homocarnosine, anserine, and histidine inhibited Fe (Ⅲ) + AA-induced bovine erythrocyte hemolysis and methemoglobin formation. These results indicate that carnosine, homocarnosine, and anserine have a comparable antioxidant activity, probably due to the histidine moiety of these compounds.
인공지능 문자 인식 모델을 통해 추출된 텍스트로, 일부 오타나 오류가 포함될 수 있으나 지속적으로 개선 중입니다.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
최근 본 자료 전체보기
UCI(KEPA) : I410-ECN-0101-2009-513-013745890
