 |
 |
 |
 |
 |
||
 |
||
 |
ON CANCER, |
|
|
|||
|
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. |
|||
|
|||
|
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 ß-synthase (CßS) 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 CßS
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 CßS-deficient patients, treatment that lowered the markedly elevated pretreatment
homocysteine level (from 337 to 72 and from 298 to 50 µmol/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.
|
|||
|
|||
|
|||
|
|||
|
|||
|
|||
|
|||
|
Enter supporting content here
INTERNAL SITE SEARCH ENGINE by Google
^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^ |
|||