Hirano H, Hamajima S, Horiuchi S, Niitsu Y, Ono S
Int J Vitam Nutr Res. 1983;53(4):377-82.
The level of NADPH-cytochrome c reductase, glutathione reductase and hepatic B2 was significantly decreased in rats fed a B2-deficient diet. The synthesis of ester forms of B2 was decreased more in the lenses of rats fed this diet for 8 weeks than in those fed this diet for 4 weeks. The glutathione reductase activity in the lens decreased as the duration of a B2-deficient diet increased; this may be ascribable to a decrease in the formation in the lenticular riboflavin ester as a coenzyme. The level of lipid peroxides increased in the serum and lenses of rats on the B2-deficient diet, however, compared to the controls, the changes in the activities of superoxide dismutase and glutathione S-transferase were not significant. Lenticular glutathione peroxidase activity was decreased significantly in rats fed the B2-deficient diet for 8 weeks. We suggest that B2 deficiency brings about metabolic disorders in the redox system to maintain lens transparency, that lipoperoxide is accumulated, and that the efficiency of the scavenging system and the activities of glutathione peroxidase and reductase are decreased.
喂食缺乏核黄素(B2)饮食的大鼠,其NADPH - 细胞色素c还原酶、谷胱甘肽还原酶和肝脏B2水平显著降低。喂食该缺乏B2饮食8周的大鼠晶状体中,B2酯形式的合成减少程度比喂食4周的大鼠更明显。晶状体中的谷胱甘肽还原酶活性随着缺乏B2饮食持续时间的增加而降低;这可能归因于作为辅酶的晶状体核黄素酯形成减少。与对照组相比,缺乏B2饮食的大鼠血清和晶状体中脂质过氧化物水平升高,然而超氧化物歧化酶和谷胱甘肽S - 转移酶活性的变化并不显著。喂食缺乏B2饮食8周的大鼠晶状体谷胱甘肽过氧化物酶活性显著降低。我们认为,B2缺乏会导致维持晶状体透明度的氧化还原系统出现代谢紊乱,导致脂过氧化物积累,清除系统效率以及谷胱甘肽过氧化物酶和还原酶活性降低。