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- W133028475 abstract "Carbon monoxide (CO) is generated from the degradation of heme, in a reaction that is catalyzed by heme oxygenase, a heat shock protein (HSP32). Loss of appetite, confusion, lethargy, and systemic organ failure are all amongst the well documented adverse effects of chronic, subhypoxic, exogenous CO poisoning, and heme treatment has been shown to accelerate hemorrhage induced circulatory collapse. Accordingly, we wanted to determine if chronic elevations in endogenous CO, from heme alone, would affect appetite, activity and survival. Towards this end, rats (N=24) were treated with heme (15 or 45μmol/Kg heme as heme-lysinate, IP q24h) for up to four weeks. Heme treatments produced up to a 3-fold increase in expired CO, which was accompanied by a transient reduction in food intake, cessation of weight gain and a >95% decrease in wheel running activity. While both heme doses produced these adverse effects, heme administration of 45μmol/Kg per day also led to circulatory collapse and premature deaths in otherwise healthy unbled rats (50% at 14 days). Concurrent provision of high zinc diet (0.5%) -which promotes formation of ZnPP, a heme oxygenase inhibitor- conferred marked improvement against heme treatments. We conclude that heme drives heme oxygenase activity to increase endogenously formed CO and produce adverse effects which can promote circulatory collapse. Jointly supported by NIH/DOD grant HL64577 (RAJ) and National Trauma Institute" @default.
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- W133028475 date "2008-03-01" @default.
- W133028475 modified "2023-09-26" @default.
- W133028475 title "Chronic heme promotes sustained elevations in CO excretion, anorexia, attenuated physical activity and circulatory collapse in rats" @default.
- W133028475 doi "https://doi.org/10.1096/fasebj.22.1_supplement.1227.10" @default.
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