Benfotiamine reduces genomic damage in peripheral lymphocytes of hemodialysis patients

被引:43
作者
Schupp, Nicole [1 ,2 ]
Dette, Eva Maria [2 ]
Schmid, Ursula [2 ]
Bahner, Udo [3 ]
Winkler, Michaela [2 ]
Heidland, August [4 ]
Stopper, Helga [2 ]
机构
[1] Univ Wurzburg, Dept Toxicol, D-97078 Wurzburg, Germany
[2] Univ Wurzburg, Dept Pharmacol & Toxicol, D-97078 Wurzburg, Germany
[3] Kuratorium Dialysis & Kidney Transplantat, D-97078 Wurzburg, Germany
[4] Univ Wurzburg, Dept Internal Med, D-97078 Wurzburg, Germany
关键词
micronuclei; vitamin B1; benfotiamine; advanced glycation end products; transketolase; plasma antioxidant capacity;
D O I
10.1007/s00210-008-0310-y
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Hemodialysis patients have an elevated genomic damage in peripheral blood lymphocytes (PBLs) and an increased cancer incidence, possibly due to accumulation of uremic toxins like advanced glycation end products (AGEs). Because the vitamin B1 prodrug benfotiamine reduces AGE levels in experimental diabetes, and dialysis patients often suffer from vitamin B1 deficiency, we conducted two consecutive studies supplementing hemodialysis patients with benfotiamine. In both studies, genomic damage was measured as micronucleus frequency of PBLs before and at three time-points after initiation of benfotiamine supplementation. AGE-associated fluorescence in plasma, and in the second study additionally, the antioxidative capacity of plasma was analyzed. Benfotiamine significantly lowered the genomic damage of PBLs in hemodialysis patients of both studies independent of changes in plasma AGE levels. The second study gave a hint to the mechanism, as the antioxidative capacity of the plasma of the treated patients clearly increased, which might ameliorate the DNA damage.
引用
收藏
页码:283 / 291
页数:9
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