Age-Related Correlation Between Antioxidant Enzymes and DNA Damage With Smoking and Body Mass Index

Thavanati, Parvathi Kumara Reddy; Kanala, Kodanda Reddy; Dios, Aurora Escoto de; Garza, Jose Maria Cantu

doi:10.1093/gerona/63.4.360

Cited by 20 publications

(10 citation statements)

References 47 publications

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“…Lipid peroxidation (oxidative injury marker), represented by malonaldehyde (MDA), is significantly correlated with body mass index (BMI) and waist circumference (4). Our data shows that, regardless of cigarette smoke exposure, obesity tended to increase levels of MDA and decrease SOD activity, classic signs of biological oxidative stress that occurs because the first antioxidant barrier (SOD) does not remove adequate serum reactive oxygen species (31,32). However, Seiva et al (33) showed that obese young male rats exposed to cigarette smoke presented increased SOD, GSH-Px and catalase enzymatic activities as a compensatory mechanism in response to cellular injury.…”

Section: Discussionmentioning

confidence: 84%

Metabolic profile and genotoxicity in obese rats exposed to cigarette smoke

Damasceno

Sinzato

Bueno

et al. 2013

Obesity

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Objective: Experimental studies have shown that exposure to cigarette smoke has negative effects on lipid metabolism and oxidative stress status. Cigarette smoke exposure in nonpregnant and pregnant rats causes significant genotoxicity (DNA damage). However, no previous studies have directly evaluated the effects of obesity or the association between obesity and cigarette smoke exposure on genotoxicity. Therefore, the aim of the present investigation was to evaluate DNA damage levels, oxidative stress status and lipid profiles in obese Wistar rats exposed to cigarette smoke. Design and Methods: Female rats subcutaneously (sc) received a monosodium glutamate solution or vehicle (control) during the neonatal period to induce obesity. The rats were randomly distributed into three experimental groups: control, obese exposed to filtered air, and obese exposed to tobacco cigarette smoke. After a 2-month exposure period, the rats were anesthetized and killed to obtain blood samples for genotoxicity, lipid profile, and oxidative stress status analyses. Results: The obese rats exposed to tobacco cigarette smoke presented higher DNA damage, triglycerides, total cholesterol, free fatty acids, VLDL-c, HDL-c, and LDL-c levels compared to control and obese rats exposed to filtered air. Both obese groups showed reduced SOD activity. These results showed that cigarette smoke enhanced the effects of obesity. Conclusion: In conclusion, the association between obesity and cigarette smoke exposure exacerbated the genotoxicity, negatively impacted the biochemical profile and antioxidant defenses and caused early glucose intolerance. Thus, the changes caused by cigarette smoke exposure can trigger the earlier onset of metabolic disorders associated with obesity, such as diabetes and metabolic syndrome.

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Section: Discussionmentioning

confidence: 84%

Metabolic profile and genotoxicity in obese rats exposed to cigarette smoke

Damasceno

Sinzato

Bueno

et al. 2013

Obesity

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“…Generation of free radicals and antioxidant capacity of the body have been observed to be modulated by environmental, physiological and nutritional factors [31] , [44] . For example, physiological factors such as aging, alteration of body mass index and obesity and life style confounding factors such as smoking, drinking and high calorie diet have enhancing effect on oxidative stress and suppressive effect on antioxidants [44] , [48] , [49] .…”

Section: Introductionmentioning

confidence: 99%

Studies on the potential protective effect of cinnamon against bisphenol A- and octylphenol-induced oxidative stress in male albino rats

et al. 2014

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Among the numerous chemicals discharged into the surrounding environment, bisphenol A (BPA) and octylphenol (OP) have been shown to increase oxidative stress in body by disturbing the prooxidant/antioxidant balance of cells. Cinnamon aqueous extract (CAE) is a natural product rich in polyphenolic compounds that have antioxidant activity. This study was designed to investigate the protective efficacy of CAE against oxidative disorders induced by BPA and OP in male albino rats. Animals were divided into 6 groups (10 rats each) and treated orally, 3 times weekly for 50 days. Group 1: control vehicle (olive oil); group 2 (25 mg BPA/kg b.wt./day); group 3 (25 mg OP/kg b.wt./day); group 4 (200 mg CAE/kg b.wt./day); group 5 (CAE 2 h before BPA administration); and group 6 (CAE 2 h before OP administration). BPA- and OP-exposed groups showed insignificant elevation in the final body weight; weight gains and significant reduction only in the relative kidneys weight. Also, BPA and OP exposure resulted in significant increase in serum urea, creatinine and kidney, brain, testicular malondialdehyde (MDA) levels. Significant reduction in tissues reduced glutathione (GSH) contents; catalase (CAT) and superoxide dismutase (SOD) activities were also recorded in BPA and OP exposed animals compared to the control vehicle group. Pretreatment with CAE 2 h either before BPA or OP administration ameliorated the BPA- and OP-induced body weight; weight gains and relative organs weight changes and biochemical adverse effects. CAE pretreatment also protected against the recorded pathological changes in kidney, brain and testis. In conclusion, CAE could ameliorate the oxidative toxic effects of BPA and OP indicating its protective antioxidant effect.

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“…Cumulating studies reported oxidative stress and inflammatory factors in smokers in cell culture ( 8 , 22 ). Reddy Thavanati et al ( 29 ) found that lymphocyte DNA damage in smokers was twofold higher than that in non-smokers and this result was associated with a reduced antioxidant capacity in smokers. In the present study, smokers and non-smokers did not show any significant difference in lymphocyte apoptosis at rest, however, smokers showed higher lymphocyte apoptosis immediately after the run at 60% VO 2max ( p <.008) and the run at 70% VO 2max ( p <.018).…”

Section: Discussionmentioning

confidence: 99%

“…Cigarettes contain more than 6,000 components, and many factors can induce DNA damage and oxidative stress in a diversity of cell types ( 6 , 17 , 18 ), which refers to a disturbance in the oxidant and antioxidant balance resulting in potential cell damage ( 2 , 22 , 29 ). In response to oxidative stress by smoking, pro-inflammatory mediators and cytokines such as TNF-α, IL-1, and IL-8 can activate the transcription factors such as activator protein-1 and NF-κB, and finally can induce apoptosis ( 2 , 8 ).…”

Section: Introductionmentioning

confidence: 99%

“…However, we do not know whether moderate intensity exercise enhances immunity in chronic cigarette smokers. Since chronic smokers have antioxidant imbalance and immune suppression ( 2 , 22 , 29 ) an additional stress (exercise) may aggravate their condition instead of inducing potentially beneficial adaptation. In addition, the exercise intensity for untrained healthy people to avoid from immune suppression is equivocal.…”

Section: Introductionmentioning

confidence: 99%

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Lymphocyte Apoptosis in Smokers and Non-Smokers Following Different Intensity of Exercises and Relation with Lactate

Park¹,

Lee²

2011

Medicine &Amp; Science in Sports &Amp; Exercise

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Purposes of this study were 1) to examine the exercise intensity where lymphocyte apoptosis index (AI) is significantly increased in smokers and non-smokers, 2) to find out whether AI is associated with level of lactate (L). Fourteen healthy untrained smokers (≤ 1 pack year, n=7) and non-smokers (n=7) aged 18 to 26 were recruited. Each subject conducted three treadmill runs at different intensities randomly. Running distance for all three runs was equivalent to 30 minute run at 70% VO2max. AI and L were analyzed at rest (Pre), immediately after (Post), and 1 h following (1 h post) each run. Data was analyzed using two way repeated measures ANOVA. Smokers showed higher AI than non-smokers at Post in 60% (12.5±0.62% vs. 9.97±0.51, p<.008) and 70% VO2max running trials (17.53±0.57% vs. 15.6±0.41, p<.018). All L values at post showed significantly higher than Pre and 1 h post, but there was no significant difference between smokers and non-smokers. The strong positive relationship between AI and L was detected (r=.739, smokers vs. r=.793, non-smokers). Smokers tend to have higher AI than non-smokers following runs at 60% and 70% VO2max, but not following a run at 80% VO2max. An increase in AI following a run at 60% VO2max indicates that lymphocyte apoptosis can be increased following moderate intensity exercise. Since L and AI at post were increased in dose-dependent manner to exercise intensity, it is suggested that an increase in lactate production during exercise might contribute to the increase in lymphocyte apoptosis.

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Age-Related Correlation Between Antioxidant Enzymes and DNA Damage With Smoking and Body Mass Index

Cited by 20 publications

References 47 publications

Metabolic profile and genotoxicity in obese rats exposed to cigarette smoke

Metabolic profile and genotoxicity in obese rats exposed to cigarette smoke

Studies on the potential protective effect of cinnamon against bisphenol A- and octylphenol-induced oxidative stress in male albino rats

Lymphocyte Apoptosis in Smokers and Non-Smokers Following Different Intensity of Exercises and Relation with Lactate

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