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甲磺酸甲酯对正常细胞和着色性干皮病细胞中紫外线修复的灭活作用。

Inactivation of ultraviolet repair in normal and xeroderma pigmentosum cells by methyl methanesulfonate.

作者信息

Cleaver J E

出版信息

Cancer Res. 1982 Mar;42(3):860-3.

PMID:7059984
Abstract

Excision repair of ultraviolet damage in the DNA of normal and xeroderma pigmentosum (Groups C, D, and variant) cells was inactivated by exposure of cells to methyl methanesulfonate immediately before irradiation independent of the presence of 0 to 10% fetal calf serum. The inactivation could be represented by a semilog relationship between the amount of repair and methyl methanesulfonate concentration up to approximately 5 mM. The inactivation can be considered to occur as the result of alkylation of a large (about 10(6) daltons) repair enzyme complex, and the dose required to reduce repair to 37% for most cells types was between 4 and 7 mM. No consistent, large difference in sensitivity to methyl methanesulfonate was found in any xeroderma pigmentosum complementation group compared to normal cells, implying that reduced repair in these groups may be caused by small inherited changes in the amino acid composition (i.e., point mutations or small deletions) rather than by losses of major components of the repair enzyme complex.

摘要

正常细胞和着色性干皮病(C组、D组及变异型)细胞DNA中紫外线损伤的切除修复,在照射前立即将细胞暴露于甲磺酸甲酯时会被灭活,这与0至10%胎牛血清的存在无关。这种灭活可以用修复量与甲磺酸甲酯浓度之间的半对数关系来表示,直至约5 mM。这种灭活可被认为是由于一种大型(约10⁶道尔顿)修复酶复合物的烷基化所致,对于大多数细胞类型,将修复降低至37%所需的剂量在4至7 mM之间。与正常细胞相比,在任何着色性干皮病互补组中均未发现对甲磺酸甲酯的敏感性存在一致的、较大差异,这意味着这些组中修复减少可能是由氨基酸组成的微小遗传变化(即点突变或小缺失)引起的,而不是由修复酶复合物主要成分的缺失所致。

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