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| Year : 2019 | Volume
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| Issue : 2 | Page : 219-225 |
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| Superoxide dismutase, glutathione peroxidase, and catalase antioxidant enzymes in chronic tobacco smokers and chewers: A case–control study |
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Poonam Agarwal1, Anjana Bagewadi2, Vaishali Keluskar2, DP Vinuth3
1 Department of Oral Medicine and Radiology, Buraydah Private Dental College, Buraydah, Al Qassim, Kingdom of Saudi Arabia
2 Department of Oral Medicine and Radiology, KLE VK Institute of Dental Sciences, Belgaum, Karnataka, India
3 Department of Oral Pathology and Microbiology, Buraydah Private Dental College, Buraydah, Al Qassim, Kingdom of Saudi Arabia
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| Date of Web Publication | 29-May-2019 |
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 Abstract | | |
Objective: Tobacco has a time dependent effect on the antioxidant system of the body. This study was designed to determine and compare alteration in levels of erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) in blood subgroups of tobacco smokers and chewers with controls. Materials and Methods: Blood samples were collected from 30 tobacco smokers (> 20 cigarettes daily), 30 tobacco chewers (> 10 packets gutka daily) and 30 controls. These groups were further divided into three subgroups (n=10) based on duration of habit (<5 yrs, 5-10 yrs, >10 yrs). The level of erythrocyte SOD, GPx and CAT were measured using standard procedures. Results: The SOD and CAT levels were significantly decreased in all subgroups of smokers and chewers whereas GPx level was significantly increased. Positive correlation was observed between SOD, GPx and CAT levels with change in duration of habit in all subgroups. No significant difference observed in SOD and CAT activity between tobacco smokers and chewers. Conclusions: The findings suggested that antioxidative enzyme activities have significant correlation with change in the duration of tobacco use. Measurement of markers of free radical activity might be useful for estimating the level of oxidative stress caused by tobacco use. Keywords: Enzymatic antioxidants, free radicals, oxidative stress, tobacco
How to cite this article:
Agarwal P, Bagewadi A, Keluskar V, Vinuth D P. Superoxide dismutase, glutathione peroxidase, and catalase antioxidant enzymes in chronic tobacco smokers and chewers: A case–control study. Indian J Dent Res 2019;30:219-25 |
How to cite this URL:
Agarwal P, Bagewadi A, Keluskar V, Vinuth D P. Superoxide dismutase, glutathione peroxidase, and catalase antioxidant enzymes in chronic tobacco smokers and chewers: A case–control study. Indian J Dent Res [serial online] 2019 [cited 2023 Mar 27];30:219-25. Available from: https://www.ijdr.in/text.asp?2019/30/2/219/259216 |
| Introduction | |  |
Tobacco use is the single most important preventable cause of illness and death. Its use is a serious public health problem worldwide with increased mortality and morbidity.[1] The WHO estimated that worldwide tobacco use causes >5 million deaths/year, and current trends show that the tobacco use will cause >8 million deaths annually by 2030.[2] Numerous scientific studies have been conducted for over half a century to determine health hazards with tobacco use. The trend of the evidence has been consistent and unambiguous about the health hazards of tobacco.
In India, 194 million men and 45 million women use tobacco in smoked or smokeless form. Only, 20% of the tobacco consumed in India by weight is consumed as cigarettes, 40% consumed as bidi, and the rest in smokeless forms.[3]
Smoking has been strongly implicated as a risk factor for chronic obstructive pulmonary disease, cancer, and atherosclerosis.[4] Convincing laboratory animal and human studies have revealed a relationship between tobacco smoke constituents, carcinogen-DNA adduct formation, and cancer.[5] As cigarette smoke is known to contain a large number of oxidants, it has been hypothesized that many of the adverse effects of smoking may result from oxidative damage to critical biological substances. Such damage could result both from oxidants present in cigarette smoke and from the activation of phagocytic cells that generate reactive oxygen species (ROS).[6] Biological effects of these highly reactive compounds are controlled in vivo by a wide spectrum of antioxidant mechanisms.[7]
Smokeless tobacco, available as snuff or chewing tobacco, has deleterious effects which are perhaps not as well known as those produced by smoking. Approximately twice the amount of nicotine is absorbed per dose from smokeless tobacco than from cigarettes, and orally absorbed nicotine also stays longer in the bloodstream.[8] Furthermore, smokeless tobacco extract is more toxic than nicotine regarding their respective oxidative stress actions and produces oxidative tissue damage and apoptosis.[9] Its use causes a number of noncancerous oral conditions, periodontal disease, delayed wound healing, and dental caries. As reviewed in detail, in the 1986 Surgeon General's report on the Health Consequences of Using Smokeless Tobacco, it is said that there is convincing evidence that smokeless tobacco use causes cancer of the oral cavity.[10]
Small amounts of ROS are constantly generated in aerobic organisms in response to both external and internal stimuli. Low levels of ROS may be indispensable in a plethora of processes.[11] In contrast, high doses of ROS produced from tobacco use result in excessive oxidative stress, which may cause severe metabolic malfunctions, and damage to biological macromolecules.[12] A wide array of enzymatic and nonenzymatic antioxidant defenses exist, including superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione reductase, beta-carotene, and Vitamin A and C and E.[13] There is an interrelationship between both activities and the intracellular levels of these metabolites, protecting themselves from oxygen toxicity. The most important enzymatic antioxidants are SOD, which catalyzes dismutation of the superoxide anion (O2−) into H2O2, which is then deactivated to H2O by CAT and GPx.[14]
Several steps have been taken worldwide through an extensive mass media propaganda whereby public have been warned of the possible health hazard of smoking. In USA, it is already yielding results. Situation in India is not encouraging.[15] The famous slogan “smoking kills–Tobacco causes cancer,” found on every cigarette pack is only confined to cigarette pack. This may be partially due to the lower literacy rate and lack of health awareness. More than this, it is due to dependence produced by nicotine.[16] Nicotine is the principal constituent of tobacco responsible for its addictive character. The 1988 Surgeon General's report concluded that nicotine was an addictive drug, similar to heroin and cocaine.[17] Addicted smokers regulate their nicotine intake and blood levels by adjusting the frequency and intensity of their tobacco use both to obtain the desired psychoactive effects and to avoid withdrawal effects.[18]
Cigarette smoking and tobacco chewing are very common in North Karnataka, especially in Belgaum district as tobacco is grown extensively in this area. Hence, particular attention is required regarding public health interventions. Wide inter individual variations exist in the antioxidant capacity which affects the susceptibility to deleterious oxidative reactions. The purpose of this study was to assess and compare the activities of erythrocytic SOD, GPx, and CAT in a sample population consisting of current smokers and chewers with controls.
| Materials and Methods | | |
After the Ethical Committee of KLE University approved the protocol, the patients visiting the Department of Oral Medicine at KLE VK Institute of Dental Sciences were asked to participate in this study (based on the inclusion and exclusion criteria). Patients who were generally healthy and had not been taking any medication for any systemic disease for at least 3 months were included in the study.
Information on smoking and chewing behavior was obtained from an interview and categorized as “smoker” or “chewer.” They were further categorized into three subgroups (<5 years, 5–10 years, and >10 years) based on the duration of habit. Patients (n = 30) who smoked >20 cigarettes daily and chewers (n = 30) who had more than 10 packets gutkha daily were selected and categorized into three subgroups (<5 years, 5–10 years, and >10 years) based on the duration of habit. Patients with no history of tobacco use were included in the control group (n = 30). The participants were fully informed of the nature of the study and written consent forms were obtained from all participants.
Smokers were instructed to refrain from smoking for the 1 h period before reporting to the laboratory as previously suggested by Dietrich et al.[19]
Five milliliter of blood was collected from an antecubital vein of the patients under aseptic precautionary measures using sterile disposable syringe. Hemoglobin estimation was done, and then the remaining sample was transferred to ethylenediaminetetraacetic acid containing vial for estimating erythrocytic SOD, GPx and CAT. The blood sample was immediately sent to the Department of Clinical Biochemistry, Prabhakar Kore Hospital and Research Centre, where the blood was centrifuged, serum separated, and analysis was carried out.
Hemoglobin level was determined using Drabkin's method.[20] SOD and GPx were estimated using Ransod and Ransel kit (Randox Laboratories Ltd., Crumlin, Co. Antrim, UK), respectively. CAT was determined using Beutler E method.[21]
Statistical analysis
ANOVA was for intragroup comparisons, and post hoc Tukey's test was used in the intergroup analysis.
| Results | | |
While erythrocytic SOD and CAT was significantly (P < 0.001) decreased in all the three subgroups of smokers and chewers, the GPx level was significantly increased in all the subgroups of smokers and chewers compared to controls [Table 1]. | Table 1: Erythrocytic enzymatic antioxidants in Tobacco Smokers, Chewers and Controls
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ANOVA showed a statistically significant difference in the level of SOD (P = 0.000), GPx (P = 0.046), and CAT (P = 0.016) between the three subgroups of chewers. Similarly, it also showed a statistically significant difference in the level of SOD (P = 0.000), GPx (P = 0.042), and CAT (P = 0.047) between the three subgroups of smokers [Table 2], [Table 3], [Table 4]. | Table 2: Intergroup comparison of erythrocytic antioxidant enzymes between Tobacco Smokers, Chewers & Controls
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 | Table 3: Intra-group comparison of erythrocytic antioxidant enzymes between subgroups of Tobacco Smokers
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 | Table 4: Intra-group comparison of erythrocytic antioxidant enzymes between subgroups of Tobacco Chewers
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Post hoc Tukey's test showed that there is a statistically significant difference between the control groups and tobacco chewer (P = 0.000) and between the control group and tobacco smokers (P = 0.000); however, no significant difference was found between the SOD and CAT levels between tobacco chewers and tobacco smokers (P = 0.0888 and 0.181, respectively) [Table 5], [Table 6], [Table 7]. | Table 5: Post hoc Tuckey test for erythrocytic superoxide dismutase, glutathione peroxidise and catalase in tobacco smokers, chewers and control groups
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 | Table 6: Post hoc tuckey test for erythrocytic superoxide dismutase, glutathione peroxidise and catalase among Tobacco Chewers
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 | Table 7: Post hoc tuckey test for erythrocytic superoxide dismutase, glutathione peroxidise and catalase among Tobacco smokers
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| Discussion | | |
Even though there is fairly irrefutable evidence for oxidative stress in cigarette smokers, the simultaneous decrease in erythrocytic SOD and CAT observed in the present study is not a common finding. While some investigators observed a decrease in GPx levels, with normal CAT activity, others have recorded an increase in GPx activity with a decrease in CAT activity in the erythrocytes of smokers when compared to nonsmoking healthy individuals. It has also been reported that the activity of CAT in erythrocyte of smokers is increased with unaltered GPx activity.[20] The simultaneous decrease in activities of both these antioxidant enzymes as observed in the present study may be detrimental to the body as this can lead to the accumulation of H2O2 in their erythrocytes, making them prone to damage by iron-mediated formation of oxyradicals.
Although we cannot explain this contradictory finding, as these enzymes are found to be influenced by genetic factors it can be hypothesized that Indians are more susceptible for such changes. These paradoxical findings among smokers recorded by various investigators may also be due to the fact that some smokers do not inhale the smoke from their cigarettes. As smokers are often exposed for longer periods to cigarette smoke from other smokers, the recorded number of cigarettes smoked by an individual may be a poor estimate for the actual exposure to the smoke toxins.[22] The results from other oxidative stress parameters reemphasize the findings from a large body of evidence that has been marshaled in the past decade, to support the presence of oxidative stress in smokers. This argument is buttressed by the fact that cigarette smoke contains a plethora of potential reactive oxygen and nitrogen species.[23]
The results of this study showed that the mean erythrocytic SOD level in controls, the tobacco smokers and tobacco chewers was 1137.90 ± 88.38 U/g Hb, 897.83 ± 138.85 U/g Hb, and 901.87 ± 99.58 U/g Hb, respectively [Table 1] and [Table 2].
The mean erythrocytic SOD level in the tobacco smokers was much lower than the control group. This finding was in accordance with the finding of Yildiz et al.[22] who found a significantly lower activity of SOD in erythrocytes of tobacco smokers than in the control group (P < 0.05). However, this finding was contrary to that of Durak et al. who suggested that smoking caused no impairment in the enzymatic antioxidant defense system and did not lead to oxidant stress in the erythrocytic activities of SOD.[21] Conversely, Abou-Seif found that the erythrocytic SOD and CAT activities were elevated in smokers.[24]
Among the subgroups, the mean level of erythrocytic SOD in tobacco smokers with ≤5 years, 5–10 years, and >10 years habit was 1047.40 ± 80.21 U/g Hb, 892.50 ± 59.79 U/g Hb, and 753.60 ± 64.11 U/g Hb, respectively [Table 1]. The level of erythrocytic SOD was significantly decreased (P < 0.05) in all the groups of tobacco smokers compared to control. Our findings are in accordance with the findings of Garg N Singh et al. and Zhou et al.[25],[26] They attributed the cause of the decrease in erythrocytic SOD level to be its inactivation by hydrogen peroxide, but are contrary to the findings of B Yokus et al and Huda Kiken et al.[27],[28]
These results suggest that increased oxidative stress occurs in smokers, owing to the free radicals present in smoke. It causes a decrease in antioxidant enzyme activities and oxidant/antioxidant imbalance. The variability of the effects of smoking on antioxidant enzyme activities may be due to multiple reasons such as interaction between direct and passive smoke exposures, different smoking patterns, and differences in the compositions of cigarettes.[29]
The mean level of erythrocytic SOD in tobacco chewers was much lower compared to the control group. Our finding is in accordance with the findings of the study done by Samal et al. According to the authors, the decreased levels indicate suppressed antioxidant status due to enormous oxidative stress.[30]
The mean level of erythrocytic SOD in chewers with ≤5 years, 5–10 years, and >10 years habit was 1009.20 ± 73.30 U/g Hb, 888.00 ± 44.49 U/g Hb, and 808.40 ± 43.37 U/g Hb, respectively [Table 1]. The level of erythrocytic SOD was significantly decreased (P < 0.05) in the subgroups of chewers with an increase in the duration of habit. Our findings are in accordance with the findings of Samal and Kilinc et al. who found a significant duration-(tobacco chewing) dependent decrease in erythrocytic SOD activity.[30],[31] According to Samal et al., the decrease in erythrocytic SOD along with an increase in the duration of tobacco chewing can be attributed to the duration-dependent increase in oxidative stress due to more free-radical generation with the use of oral smokeless tobacco.[30]
The mean erythrocytic GPx level in controls, tobacco smokers, and tobacco chewers was 31.77 ± 4.97 U/g Hb, 79.23 ± 10.86 U/g Hb, and 54.93 ± 14.85 U/g Hb, respectively [Table 2].
The mean level of erythrocytic GPx in tobacco smokers was much higher compared to the control group. This finding was in accordance with the finding of Patel et al. who reported a significant elevation in levels of GPx (P = 0.017) in patients with a history of tobacco smoking compared to controls.[32] This may be due to the fact that erythrocytic GPx being the first line antioxidant enzyme is involved both in the detoxification of reactive species, H2O2, and conversion of lipid hydroperoxides into nontoxic alcohols, and its level increases to combat the increased oxidative stress.[29] Yildiz et al. also recorded an increase in erythrocytic GPx activity with a decrease in CAT activity in the erythrocytes of tobacco smokers when compared to nonsmoking healthy individuals.[22] Our findings are contrary with the findings of Kocyigit et al. and Hemalatha et al. who found a decrease in the level of GPx with tobacco use.[20],[33] In addition, Durak et al. found no changes in the level of GPx in patients with a history of tobacco use. They concluded that the tobacco use does not lead to oxidant stress in the erythrocytes, possibly because these cells have potent antioxidant defense capacity.[21]
Among the subgroups of tobacco smokers with ≤5 years, 5–10 years, and smokers >10 years of habit, erythrocytic GPx was in the range of 74.40 ± 10.61 U/g Hb, 83.60 ± 7.96 U/g Hb, and 79.70 ± 14.09 U/g Hb, respectively [Table 1]. The level of erythrocytic GPx was significantly increased (P < 0.05) in the subgroups of tobacco smokers with increase in the duration of habit. This could be due to the fact that the erythrocytic GPx being the first line antioxidant enzyme involved in the detoxification of reactive species, and its level increases to combat the increased oxidative stress with an increase in the duration of habit.[24]
The mean erythrocytic CAT level in controls, tobacco smokers, and tobacco chewers was 616.07 ± 17.42 U/g Hb, 556.90 ± 7.66 U/g Hb, and 548.80 ± 35.56 U/g Hb, respectively [Table 2].
The mean level of erythrocytic CAT in tobacco smokers was 556.90 ± 7.66 which was much lower compared to the control group, i.e., 616.07 ± 17.42 U/g Hb. This is consistent with the findings of Hemalatha et al.[20] Durak et al. found no changes in the level of CAT in patients with history of tobacco use. According to the authors, smoking causes no impairment in the enzymatic antioxidant defense system as erythrocytes have a potent defense capacity.[21]
Among the subgroups of tobacco smokers with a habit of ≤5 years, 5–10 years, and >10 years, erythrocytic CAT level was in the range of 539.30 ± 6.17 U/g Hb, 555.00 ± 8.14 U/g Hb, and 576.40 ± 8.62 U/g Hb, respectively [Table 7]. The level of erythrocytic CAT was significantly decreased (P < 0.05) in all the groups of tobacco smokers compared to control. Our findings are consistent with the findings of A Hemalatha et al., Yildiz L et al., Zhou JF et al and B Yokus et al.[20],[22],[26],[27]
Conversely, Durak et al. study results suggested that tobacco smoking caused no impairment in the level of erythrocytic CAT. The authors therefore concluded that tobacco smoking does not lead to oxidant stress in the erythrocytes, possibly because these cells have potent antioxidant defense capacity.[21]
Among tobacco chewers, it was found that the erythrocytic CAT level was significantly decreased (P < 0.05) in all the subgroups of tobacco chewers compared to control [Table 5]. Toth et al. and Garg N Singh et al. have shown an increase in CAT level in their study.[25],[34] Kocyigit et al., Durak et al., Abdurrahim et al., and Alejandro D Bolzan et al. have shown erythrocytic CAT value to be unchanged.[21],[28],[33],[35] According to Garg et al., the increase in CAT activity might be caused by the fact that for a given concentration of CAT, the initial rate of hydrogen peroxide removal is directly proportional to the hydrogen peroxide concentration. The enzyme CAT comes into action only after a particular concentration of hydrogen peroxide. Below the threshold concentration, CAT has no role to play. Thus, an increase in the erythrocytic catalytic activity in smokers may be caused by high level of hydrogen peroxide formation.[25]
Yokus et al. through his study showed a reduced CAT activity in tobacco smokers which according to the author may be due to oxidative inactivation of enzyme protein.[27]
Post hoc Tukey's test [Table 5], [Table 6], [Table 7] showed that there is a significant difference between the control group and the tobacco chewers (P = 0.001). Furthermore, there was statistically significant difference between control group and tobacco smokers (P = 0.001). This could be explained by the fact that the erythrocytic antioxidant enzymes of controls have no excessive ROS to counteract; hence, their alterations are not as marked as in the patients with a history of tobacco use.[24]
The insignificant difference was seen in the level of erythrocytic SOD and CAT in the intergroup comparison between tobacco smokers and chewers with post hoc Tukey's test [Table 5] and [Table 7]. This appears logical because erythrocytic CAT is thought to account for a notable part of the destruction of H2O2, which is partly generated by erythrocytic SOD.[36],[37]
In the erythrocytic GPx levels, the statistically significant difference between tobacco smokers and tobacco chewers could be attributed to the fact that smokers are often exposed for longer periods to cigarette smoke from other smokers. The recorded number of cigarettes smoked by an individual may therefore be a poor estimate for the actual exposure to the smoke toxins.[22]
A statistically significant difference was seen in the levels of erythrocytic SOD, GPx, and CAT in the intragroup comparisons between the subgroups of tobacco smokers and tobacco chewers 22 [Table 4] and [Table 6]. The sustained release of reactive free radicals of tobacco imposes an oxidant stress and perturbs the antioxidant defense systems in blood of tobacco users. The antioxidant enzymes, therefore, show more alterations with an increase in the duration of the use of tobacco.
| Conclusion | | |
The study reveals that the mean value of erythrocytic SOD and CAT was decreased in all the three subgroups of tobacco smokers and chewers, whereas the level of erythrocytic GPx was significantly increased in all the groups of tobacco smokers and chewers.
It can hence be concluded that there is an increased oxidative stress in chronic tobacco smokers and tobacco chewers as assessed by a significant decrease in the antioxidant enzymes such as erythrocytic SOD and CAT and increase in the levels of enzyme GPx. The concomitant decrease in the activities of both erythrocytic CAT and SOD raises rational grounds for expressing concern over the increased susceptibility toward oxidative stress in these patients. As a result of the changed antioxidant status in long-term tobacco users, peroxidation reactions may be accelerated and some deleterious changes may occur in their body.
At the dawn of the 21st century, we need to aim at achieving a tobacco-free society. All the health-care professionals can work together to achieve this goal and prevent major health problems. At the individual level, we should maximize access to cessation services for all tobacco users, and promote further research to improving nicotine replacement therapies and other pharmacologic approaches. Health-care professionals can raise awareness and promote cessation with every clinical opportunity. Reducing and even eliminating nicotine from tobacco are also technically feasible and may hold the future in eradicating the potential for addiction.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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Correspondence Address:
Dr. D P Vinuth
Department of Oral Pathology, Buraydah College of Pharmacy and Dentistry, Buraydah, Al Qassim
Kingdom of Saudi Arabia
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ijdr.IJDR_268_12
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7] |
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