BackgroundCardiovascular disease (CVD) remains one of the major killers in modern society. One strong risk factor of CVD is cigarette smoking that causes myocardial injury and leads to the genesis of pathological cardiovascular events. However, the exact toxic component(s) of cigarette smoke (CS) and its molecular and cellular mechanisms for causing myocardial injury leading to heart damage and its prevention are largely unknown.Methodology/Principal FindingsUsing a guinea pig model, here we show that chronic exposure to CS produces myocardial injury that is prevented by vitamin C. Male guinea pigs were fed either vitamin C-deficient (0.5 mg/day) or vitamin C-sufficient (15 mg/day) diet and subjected to CS exposure from 5 Kentucky Research cigarettes (3R4F)/day (6 days/week) in a smoke chamber up to 8 weeks. Pair-fed sham controls were subjected to air exposure instead of CS exposure under similar conditions. Myocardial injury was produced in CS-exposed marginal vitamin C-deficient guinea pigs as evidenced by release of cardiac Troponin-T and I in the serum, oxidative stress, inflammation, apoptosis, thrombosis and collagen deposition in the myocardium. Treatment of rat cardiomyocyte cells (H9c2) in vitro and guinea pigs in vivo with p-benzoquinone (p-BQ) in amounts derived from CS revealed that p-BQ was a major factor responsible for CS-induced myocardial damage. A moderately large dose of vitamin C (15 mg/day) prevented CS/p-BQ-induced myocardial injury. Population based studies indicated that plasma vitamin C levels of smokers without disease were significantly lower (p = 0,0000) than that of non-smokers. Vitamin C levels of CS-related cardiovascular patients were further lower (p = 0.0000) than that of smokers without disease.Conclusions/SignificanceThe results indicate that dietary supplementation of vitamin C may be a novel and simple therapy for the prevention of pathological cardiovascular events in habitual smokers.
Cigarette smoke (CS) causes oxidative damage and tea polyphenols have strong antioxidant properties. Therefore, we studied the effect of a black tea (BT) infusion on CS-induced oxidative damage of proteins both in vitro and in vivo. In the in vitro experiment, bovine serum albumin (BSA) or a guinea pig tissue microsomal suspension was incubated with an aqueous extract of CS (CS-solution) in the presence or absence of the BT infusion. Protein oxidation was measured by immunoblotting of the dinitrophenylhydrazone derivatives of the protein carbonyls followed by densitometric scanning. Protein degradation was assessed by SDS-PAGE. BT prevented (P < 0.05) CS-induced oxidation of BSA and oxidative degradation of guinea pig lung, liver and heart microsomal proteins. This was also observed when the BT infusion was replaced by its components, i.e, flavonols, theaflavins, thearubigins and catechins. BT prevented microsomal protein degradation by inhibiting oxidative modification of the proteins. The antioxidant effect of BT was similar to that of green tea. In the in vivo experiment, partially ascorbate-deficient guinea pigs were subjected to CS exposure from 5 cigarettes/(guinea pig. d) for 7 d and given water or the BT infusion (20 g/L) to drink. Guinea pigs exposed to CS and given water had extensive oxidation accompanied by 39, 40 and 30% losses (P < 0.05) of microsomal proteins of lung, liver and heart, respectively. However, when the CS-exposed guinea pigs consumed the BT infusion instead of water, the oxidation of microsomal proteins was reduced (P < 0.05) approximately 90, 97 and 70% in lung, liver and heart, respectively. Protein loss was reduced (P < 0.05) approximately 92, 98 and 90% in lung, liver and heart, respectively. The results, if extrapolated to humans, would indicate that regular intake of tea may protect smokers from CS-induced oxidative damage and consequent degenerative diseases.
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