Sivak A, Rudenko L, Teague L G
Environ Mutagen. 1982;4(2):143-62. doi: 10.1002/em.2860040206.
The influence of caffeine on cytotoxicity and postreplication repair of DNA was examined following exposure of several cell types to physical and chemical agents known to damage DNA. The cell types used in this study were normal human fibroblasts (HS-WP), human xeroderma pigmentosum fibroblasts (SGL), Chinese hamster V79 cells, mouse BALB/c-3T3 cells, and secondary Syrian hamster embryo cells. The DNA damaging agents were ultraviolet light (UV), N-2-acetoxy-fluorenylacetamide (AFAA), nitroquinoline-N-oxide (NQO) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). Induction of cytotoxicity in Chinese hamster V79 cells due to ultraviolet light or AFAA exposure was enhanced by caffeine at a concentration of 1.0 mM in the culture medium, but not at 0.2 or 0.05 mM. Caffeine also inhibited postreplication repair in these cells at the same concentrations. In contrast, postreplication repair was not affected by caffeine at concentrations up to 1.0 mM in normal human fibroblasts (HS-WP), human xeroderma pigmentosum fibroblasts (SGL), secondary Syrian hamster embryo cells, and mouse BALB/c-3T3 cells following treatment with ultraviolet light, AFAA, NQO, or MNNG. Cytotoxicity in BALB/c-3T3 cells following exposure to ultraviolet light or AFAA was enhanced in the presence of caffeine at 1.0 or 0.2 mM, although these concentrations of caffeine had no effect on postreplication repair in these cells. The inhibitory effect of caffeine on postreplication repair was found only in Chinese hamster V79 cells among the five cell types used in this study. Both normal and xeroderma pigmentosum human cells repaired mutagen-induced DNA damage equally well in the absence or presence of caffeine at concentrations of 1.0 mM or less.
在几种细胞类型暴露于已知会损伤DNA的物理和化学试剂后，研究了咖啡因对DNA细胞毒性和复制后修复的影响。本研究中使用的细胞类型包括正常人成纤维细胞（HS-WP）、人类着色性干皮病成纤维细胞（SGL）、中国仓鼠V79细胞、小鼠BALB/c-3T3细胞和叙利亚仓鼠胚胎二代细胞。DNA损伤剂为紫外线（UV）、N-2-乙酰氧基-芴基乙酰胺（AFAA）、硝基喹啉-N-氧化物（NQO）和N-甲基-N'-硝基-N-亚硝基胍（MNNG）。在培养基中浓度为1.0 mM的咖啡因可增强中国仓鼠V79细胞因紫外线或AFAA暴露而诱导的细胞毒性，但在0.2或0.05 mM时则无此作用。咖啡因在相同浓度下也抑制这些细胞的复制后修复。相比之下，在正常人成纤维细胞（HS-WP）、人类着色性干皮病成纤维细胞（SGL）、叙利亚仓鼠胚胎二代细胞和小鼠BALB/c-3T3细胞经紫外线、AFAA、NQO或MNNG处理后，浓度高达1.0 mM的咖啡因对复制后修复没有影响。在1.0或0.2 mM咖啡因存在的情况下，BALB/c-3T3细胞暴露于紫外线或AFAA后的细胞毒性增强，尽管这些浓度的咖啡因对这些细胞的复制后修复没有影响。在本研究使用的五种细胞类型中，仅在中国仓鼠V79细胞中发现咖啡因对复制后修复有抑制作用。在浓度为1.0 mM或更低的咖啡因存在或不存在的情况下，正常人和着色性干皮病人类细胞对诱变剂诱导的DNA损伤修复效果相同。
