Abstract
Differences between reactive oxygen species and antioxidant defense system unbalance the redox status. The exposure to cigarette smoke can increase this imbalance. Trans-resveratrol is a polyphenol with great antioxidant action that reduces the oxidative stress. This study investigated the effect of the trans-resveratrol supplementation on the cardiac oxidative stress in rats exposed to cigarette smoke. Male Wistar rats were randomized into four groups: Control Group (CG), Exposure to Smoke Group (ESG), Antioxidant Group (AG) and Exposure to Smoke plus Antioxidant Group (ESAG). Animals were exposed to cigarette smoke and supplemented with trans-resveratrol (6.0 mg kg -1 ) for two months. The lipid peroxidation (TBARS) and the enzymatic activity of catalase (CAT) were measured in the cardiac muscle. The ESG presented the highest lipid peroxidation level compared with CG (p < 0.001), AG (p < 0.001) and ESAG (p < 0.006). The CAT activity was higher in the AG (p < 0.001) and ESAG (p < 0.001) compared with CG. The ESG presented lower CAT activity compared with the ESAG (p < 0.001). The supplementation of Trans-resveratrol attenuated the cardiac oxidative stress and increased the activity of catalase. Our findings evidenced the cardioprotective effect of trans-resveratrol in rats exposed to cigarette smoke.
Highlights
Smoking is one of the leading risk factors for non-communicable diseases, such as cardiovascular disease, diabetes, chronic respiratory diseases, and cancer (WHO, 2012)
After one week of adaptation to individual cages, animals were divided into four groups: Control Group (CG), Exposure to Smoke Group (ESG), Antioxidant Group (AG) and Exposure to Smoke plus Antioxidant Group (ESAG)
Data expressed as mean ± standard deviation; CG - Control Group; ESG Exposure to Smoke Group; AG - Antioxidant Group; ESAG - Exposure to Smoke plus Antioxidant Group; * - Significant difference before vs. after
Summary
Smoking is one of the leading risk factors for non-communicable diseases, such as cardiovascular disease, diabetes, chronic respiratory diseases, and cancer (WHO, 2012). The ROS and nitrogen may lead to a macromolecular damage and potential imbalance of redox pairs via deregulation of the cellular signaling pathways (JONES, 2006). All cell components and main biomolecules (lipids, proteins, nucleic acids) are susceptible to oxidative damage and can suffer change in the structure and function (THÉROND et al, 2000). This contributes to the development and/or progression of the diseases associated with smoking (WHO, 2012), exposure to cigarette smoke (OBERG et al, 2011), and cardiovascular dysfunctions such as atherosclerosis, ischemia-reperfusion injury, chronic ischemic heart disease, cardiomyopathy, congestive heart failure, and arrhythmias (TAVERNE et al, 2013)
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