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THE CHEMICAL CAUSE OF CORONARY DISEASE IN SMOKERS

 

CARBON MONOXIDE:

Cigarette smoking causes the largest human exposure to carbon monoxide.  The COHb [C = carbon, O = oxygen, CO = carbon monoxide, Hb = hemoglobin] content in an average nonsmoker is about 0.5%, while in a smoker it is ten time3s higher, about 5% (but level up to 12% have been reported).  Toxics A to Z, Jim Harte et al, U. of Cal. Press, 1991, p. 25.

 

Lowered level of hemoglobin is minor compared to its effect upon the arteries.  The formation of plack is primarily a healing response brought on by reactive chemicals.  What clogs the arties is not just cholesterol, but also includes cells from the artery wall.  The principle reactive chemical from smoking is carbon monoxide.  Carbon monoxide is the principle culprit that accounts for why a person who averages a pack or more a day is over two-and-one half times more likely in any given year to die of a coronary disease.  Given the prevalence early from tobacco because of coronary problems than they do from cancer. 

It was in April of 1979 in Scientific American that an article presented the evidence in an organized way on the link to carbon monoxide with coronary disease.  That evidence still stands. 

 

 

 

Vascular Biology

Relationship Between Homocysteine and Superoxide Dismutase in Homocystinuria

Possible Relevance to Cardiovascular Risk

David E. L. Wilcken; Xing Li Wang; Tetsuo Adachi; Hirokazu Hara; Natalia Duarte; Kathryn Green; Bridget Wilcken

From the Department of Cardiovascular Medicine (D.E.L.W., X.L.W., N.D.), Prince of Wales Hospital, and University of New South Wales Centre for Thrombosis and Vascular Research, Sydney, Australia; the Laboratory of Clinical Pharmaceutics (T.A., H.H.), Gifu Pharmaceutical University, Gifu, Japan; and the NSW Biochemical Genetics Service (K.G., B.W.), the Royal Alexandra Hospital for Children, Sydney, Australia.

Correspondence to Professor David Wilcken, Cardiovascular Genetics Laboratory, Edmund Blacket Building, Prince of Wales Hospital, Randwick, NSW 2031, Australia. E-mail d.wilcken@unsw.edu.au

AbstractA modest homocysteine elevation is associated with an increased cardiovascular risk. Marked circulating homocysteine elevations occur in homocystinuria due to cystathionine -synthase (CS) deficiency, a disorder associated with a greatly enhanced cardiovascular risk. Lowering homocysteine levels reduces this risk significantly. Because homocysteine-induced oxidative damage may contribute to vascular changes and extracellular superoxide dismutase (EC-SOD) is an important antioxidant in vascular tissue, we assessed EC-SOD and homocysteine in patients with homocystinuria. We measured circulating EC-SOD, total homocysteine (free plus bound), and methionine levels during the treatment of 21 patients with homocystinuria, 18 due to CS deficiency, aged 8 to 59 years, and 3 with remethylating defects. We measured total homocysteine by immunoassay, EC-SOD by ELISA, and methionine by amino acid analysis and assessed interindividual and intraindividual relationships. There was a significant, positive relationship between EC-SOD and total homocysteine. For the interindividual assessment, levels were highly correlated, r=0.746, N=21, P<0.0001. This relationship was maintained after taking into account intraindividual patient variation (r=0.607, N=62, P<0.0001). In 2 newly diagnosed CS-deficient patients, treatment that lowered the markedly elevated pretreatment homocysteine level (from 337 to 72 and from 298 to 50 mol/L) reduced the associated elevated EC-SOD in each by 50%. EC-SOD and methionine levels were unrelated (r=0.148, n=39, P=0.368). The positive relationship between circulating EC-SOD and homocysteine could represent a protective antioxidant response to homocysteine-induced oxidative damage and contribute to reducing cardiovascular risk in homocystinuric patients.  EC-SOD levels may be relevant to the pathogenesis of vascular disease in other patient groups.


Key Words: homocysteine superoxide dismutase oxidative stress vascular disease cystathionine -synthase deficiency

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Disclaimer:  The information, facts, and opinions provided here is not a substitute for professional advice.  It only indicates what JK believes, does, or would do.  Always consult your primary care physician for medical advice, diagnosis, and treatment.