Specific activity of methionine sulfoxide reductase in CD-1 mice is significantly affected by dietary selenium but not zinc |
| |
Authors: | Eric O Uthus Jackob Moskovitz |
| |
Institution: | (1) US Department of Agriculture, ARS, Grand Forks HumanNutrition Research Center, 58202 Grand Forks, ND;(2) Department of Pharmacology and Toxicology, The University of Kansas, School of Pharmacy, 66045-7582 Lawrence, KS |
| |
Abstract: | Reactive oxygen species-mediated oxidation of methionine residues in protein results in a racemic mixture of R and S forms
of methionine sulfoxide (MetO). MetO is reduced back to methionine by the methionine sulfoxide reductases MsrA and MsrB. MsrA
is specific toward the S form and MsrB is specific toward the R form of MetO. MsrB is a selenoprotein reported to contain
zinc (Zn). To determine the effects of dietary selenium (Se) and Zn on Msr activity, CD-1 mice (N=16/group) were fed, in a
2×2 design, diets containing 0 or 0.2 μg Se/g and 3 or 15 ∥ Zn/g. As an oxidative stress, half of the mice received L-buthionine
sulfoximine (BSO; ip; 2 mmol/kg, three times per week for the last 3 wk); the others received saline. After 9.5 wk, Msr (the
combined specific activities of MsrA and MsrB) was measured in the brain, kidney, and liver. Se deficiency decreased (p<0.0001)
Msr in all three tissues, but Zn had no direct effect. BSO treatment was expected to result in increased Msr activity; this
was not seen. Additionally, we found that the ratio of MetO to methionine in liver protein was increased (indicative of oxidative
damage) by Se deficiency. The results show that Se deficiency increases oxidation of methionyl residues in protein, that Se
status affects Msr (most likely through effects on the selenoprotein MsrB), and that marginal Zn deficiency has little effect
on Msr in liver and kidney. Finally, the results show that the oxidative effects of limited BSO treatment did not upregulate
Msr activity. |
| |
Keywords: | Methionine sulfoxide reductase mice oxidation selenium deficiency zinc |
本文献已被 PubMed SpringerLink 等数据库收录! |
|