Shimoi K, Akaiwa E, Mori N, Sano M, Nakamura Y, Tomita I
Laboratory of Health Science, School of Pharmaceutical Sciences, University of Shizuoka, Japan.
Mutat Res. 1992 Apr;266(2):205-13. doi: 10.1016/0027-5107(92)90188-8.
Pyridoxal (PL) and pyridoxal 5'-phosphate (PLP) showed a marked bio-antimutagenic effect on UV-induced mutagenesis in E. coli B/r WP2, but not in the DNA excision repair-deficient strain WP2suvrA under the condition where no cellular toxicity was observed. No delay in the first cell division was seen on post-treatment with PL after UV irradiation. PL reduced not only UV- but 4-nitroquinoline-1-oxide-induced mutation, while it was ineffective in N-methyl-N'-nitro-N-nitrosoguanidine- or gamma-ray-treated cells. These results suggest that PL promotes DNA excision repair directly or indirectly and the decrease in the amount of unrepaired DNA damage might cause the reduction of UV-induced mutations in E. coli B/r WP2. In addition to the above observation, PLP reduced the frequency of mitomycin C- (2 mg/kg, i.p.) induced micronuclei in mouse peripheral blood cells. Simultaneous or subsequent oral administration of PLP (25 mg/kg) decreased the frequency of micronucleated peripheral reticulocytes.
吡哆醛（PL）和磷酸吡哆醛（PLP）对紫外线诱导的大肠杆菌B/r WP2中的诱变具有显著的生物抗诱变作用，但在未观察到细胞毒性的条件下，对DNA切除修复缺陷菌株WP2suvrA没有这种作用。紫外线照射后用PL处理后，首次细胞分裂没有延迟。PL不仅能减少紫外线诱导的突变，还能减少4-硝基喹啉-1-氧化物诱导的突变，而对N-甲基-N'-硝基-N-亚硝基胍或γ射线处理的细胞无效。这些结果表明，PL直接或间接促进DNA切除修复，未修复的DNA损伤量的减少可能导致大肠杆菌B/r WP2中紫外线诱导的突变减少。除上述观察结果外，PLP还降低了丝裂霉素C（2mg/kg，腹腔注射）诱导的小鼠外周血细胞微核频率。同时或随后口服PLP（25mg/kg）可降低微核化外周网织红细胞的频率。
