Environmental validation of the homocystine theory of arteriosclerosis.
It has been proposed that elevated concentrations of homocystine in vascular tissue could cause arterial damage leading to arteriosclerosis. This theory is indirectly supported by research in the area of environmental toxicology, which has revealed that carbon monoxide and carbon disulfide, agents whose prolonged exposure is known to result in the development of arteriosclerotic changes, induced vitamin B6 deficiency states which predictably lead to a homocystinuria-like state. Such information provides strong indirect support of the controversial homocystine theory of arteriosclerosis.
D000328:Adult; D000393:Air Pollutants / Q000009:adverse effects; D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology* / Q000378:metabolism; D002246:Carbon Disulfide / Q000009:adverse effects; D002248:Carbon Monoxide / Q000009:adverse effects; D002648:Child; D006579:Heterozygote; D006711:Homocystine / Q000378:metabolism*; D006712:Homocystinuria / Q000150:complications; D006801:Humans; D008875:Middle Aged; D011817:Rabbits; D012306:Risk; D026681:Vitamin B 6 Deficiency / Q000150:complications
D000393:Air Pollutants; D006711:Homocystine; D002248:Carbon Monoxide; D002246:Carbon Disulfide