20 Inadequate Vitamin Ε and Selenium Nutrition Xenobiotic Metabolism: Nutritional Effects Downloaded from pubs.acs.org by UNIV OF TEXAS AT DALLAS on 02/27/19. For personal use only.
Effect on Enzymes Associated with Hydroperoxide Metabolism C. CHANNA REDDY, CRAIG Ε. THOMAS, and RICHARD W. SCHOLZ Department of Veterinary Science and Center for Air Environment Studies, The Pennsylvania State University, University Park, PA 16802 Hydroperoxides are the immediate oxygenase products of various polyenoic fatty acids formed via the cyclooxygenase pathway and the lipoxygenase(s) path way. Not only are these semistable intermediates further metabolized to prostaglandins and leukotrienes, but they have been shown to influence various enzyme activities including cyclooxygenase, 5-lipoxygenase, etc. In addition they can be readily decomposed by transition metals to produce extremely reactive free radicals which in turn, might cause peroxidative damage to biological membranes. By sequestering free radicals and reducing hydroperoxides, dietary vitamin Ε and selenium (Se) have been implicated respectively in the protection of membranes from oxidative damage. In these studies, we have in vestigated the effects of altered vitamin Ε and/or Se nutrition on cytochrome P-450 peroxidase, prostaglandin H synthase and glutathione peroxidases (GSH-Pxs). In general, vitamin Ε deficiency had no effect on GSH-Px activities whereas opposite effects were observed on heme peroxidase (signifi cantly decreased) and PGH synthase (two fold in crease). Se deficiency resulted in a marked de crease of Se-GSH-Px activity but caused signifi cant elevation of non-GSH-Px and heme peroxidase activities. These differential effects have been interpreted as a compensatory mechanism to one another to protect cell from peroxidative damage. Recent investigations in many laboratories indicate that lipid peroxidation may be a fundamental mechanism of oxidant toxicity which can be initiated by atmospheric oxidants such as O3 and NO2 or by enzymatically produced reactive oxygen intermediates like hydroxyl radical, singlet oxygen, etc. (1-6). These short-lived oxygen intermediates can be generated by several enzymatic and non-enzymatic processes (Figure 1). It is evident from the figure that the cellular production of H2O2 seems to be a physiological 0097-6156/85/0277-0253$06.00/0 © 1985 American Chemical Society
REDUCTION
ANION)
2
2
2
2
• OH"
• -Oil • OH
3
F E * • -OH
• ll 0 ->- 0
2
2
F E * • 0,
RADICALS:
0
2
OCL-
STATE)
,
2
H 0
2
1
2
< AG)
2
no
(SINGLET OXYGEN)
2
CATALASE
2
H 0>l/2 0
SELENIUM DEPENDENT GLUTATHIONE PEROXIDASE 2H 0 • GSSG
1
2GSII
(HYDROGEN PEROXIDE)
>-
ETC
REDUCTION
.•211)
URATEOXIDASE GLYCOLATE OXIDASE D-ANINO AC D OXIDASE
