1996
DOI: 10.1172/jci118776
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The oxidant stress of hyperhomocyst(e)inemia.

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Cited by 680 publications
(456 citation statements)
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“…A possible explanation for this observation is that folate possesses antiinflammatory action by suppressing superoxide generation and enhancing nitric oxide production (Das, 2003). Several investigators have noted that folate and folic acid suppress superoxide production, and prolong a half-life of nitric oxide (Loscalzo, 1996;Das, 2001;Rossi et al, 2004). Verhaar et al (1998) demonstrated that folic acid restored and attenuated endothelial dysfunction, and endothelial dysfunction has been postulated to be part of an exaggerated maternal inflammatory response in pregnancy (Redman et al, 1999).…”
Section: Discussionmentioning
confidence: 99%
“…A possible explanation for this observation is that folate possesses antiinflammatory action by suppressing superoxide generation and enhancing nitric oxide production (Das, 2003). Several investigators have noted that folate and folic acid suppress superoxide production, and prolong a half-life of nitric oxide (Loscalzo, 1996;Das, 2001;Rossi et al, 2004). Verhaar et al (1998) demonstrated that folic acid restored and attenuated endothelial dysfunction, and endothelial dysfunction has been postulated to be part of an exaggerated maternal inflammatory response in pregnancy (Redman et al, 1999).…”
Section: Discussionmentioning
confidence: 99%
“…J. Parasitol., 10 (4): 151-159, 2015 stress through autoxidation of Hcy yielding hydrogen peroxide (Loscalzo, 1996). Thus, the elevation of Hcy in parasitized cattle in our study can also corroborate the results of preceding studies that implicate the role of oxidative stress on damaging erythrocytes and the anemia Razavi et al, 2011), as well as emphasize the probable formation of endothelial injuries and coagulation disorders (like disseminated intravascular coagulation) due to occurred hyperhomocysteinemia, which, in turn, could help the appearance of anemia.…”
Section: Discussionmentioning
confidence: 99%
“…Endothelial dysfunction, including decreased endothelial cell-dependent vasorelaxation, is increasingly proposed to be triggered by free radicals generated during auto-oxidation of homocysteine (Loscalzo, 1996). According to the work of , homocysteine auto-oxidation might prevent thiol nitrosation that, under normal physiologic conditions, sustains the antiplatelet and vasorelaxing activities of NO by increasing the stability of NO (Simon et al, 1993;Stamler et al, 1989).…”
Section: Hyperhomocysteinemia-mediated Oxidant Stress Through Imbalanmentioning
confidence: 99%