INTRODUCTION:

Tobacco is the leading cause of morbidity and mortality among the young and the elderly [1]. According to report of World Health Organization (WHO) tobacco is considered as the single greatest cause of preventable death globally [2].

Direct tobacco use is estimated to cause five million deaths a year globally, while indirect exposure leads to an additional 600, 000 deaths [3]. Tobacco consumption alters several biological parameters [4], and it has rich on pro-oxidants that are proven to induce oxidative stress [5]. Oxidative stress is defined as an imbalance in the balance between antioxidants and pro-oxidants in favor of antioxidants [6]. The inflammatory cells are then a source of free radicals in the forms of reactive oxygen and nitrogen species [7]. They are constantly generated inside cells following exposure to xenobiotics in our ambient environment [8]. It can affect cardio-vascular system, respiratory system, oral cavity, teeth etc [9]. The use of tobacco in forms other than smoking is called as smokeless tobacco (SLT) use. Chewing tobacco is the most popular form of smokeless tobacco use in different countries. Many of recent landmarks in scientific research have shown that in human beings, Oxidative stress is an important factor causing metabolic and physiological alterations and various diseases in the body [10]. Several adverse health effects have been attributed to smokeless tobacco. There is misunderstanding among people that tobacco chewing is least injurious to health [11]. ST mixtures differ according to their geographic location of use and the nature of chemicals added to them. Chewing tobacco is made up of cured tobacco leaves in the form of a plug, twist or loose leaves and is chewed in the mouth [12]. Chewing tobacco is a major risk factor for lifestyle disorders [13]. Which is believed to be a significant contributor to excess mortality [14]? The aim of our work is based on the realization of some analyses of lipid profile, biochemical and hematological biomarkers andestimation of blood pressure on Algerian men for study the effect of tobacco chewing.

Subject and methods:

Ethical approval (Appendix) was sought and approved by the Ethical Committee of the Department of Cellular and Molecular Biology, Faculty of natural sciences and life, University of El-Oued. This study was conducted on 22 volunteers man adult (mean aged 30.97±1.33 years), were divided into two groups; habitual chewers and non-smokers (11 subjects) when the mean consumption of tobacco in chewing form 37.50±3.65 grams per day and mean duration of the consumption 16.09±3.66 years, and 11 healthy volunteers served as controls, were joined in this study. All the volunteers in this study live in the El-Oued area located in the southeast of Algeria.

Inclusion Criteria:

The populations of our study included the habitual chewers for more than 5 years and non-tobacco consumers.

Exclusion Criteria:

To eliminate the factors which might affect lipid profile and biochemical parameters, we excluded all diabetic, high blood pressure and other chronic diseases subjects from chewers and healthy controlsgroups.

Laboratory Investigations:

Fasting blood samples were collected and transferred into EDTA tubes for hematological analysis and non-heparinized tubes for lipid profile and biochemical analysis. The serum was obtained by centrifugation of the blood at 3000 × rpm for 5 min and stored at -20°C until use. The samples were collected between 08:00 hours and 10:00. The determination of hematological parameters performed using fully Auto Blood Cell Counter. The following serum biochemical and lipid parameters were measured using commercial kits (Biomaghreb, Tunisia): blood sugar, serum urea, serum creatinine, aspartate aminotransferase (AST), triglyceride (TG), total cholesterol (TC) and High-Density Lipoprotein-cholesterol (HDL-c) levels. Low-Density Lipoprotein-cholesterol (LDL- c), Very Low-Density Lipoprotein-cholesterol (VLDL- c) were calculated by using Freidewald et al (1972) [15] formula: VLDL-c = TG/5; LDL-c= TC - (HDL-c + TG/5) and Atherogenic Index (AI) = TC/ HDL-caccording to Gomina et al (2013) [16].

Statistical methodology:

The statistical evaluation is carried out by the student T test using Minitab software (version 13.31). The reported data are the means of measurements and their standard error of mean (SEM) values.

RESULTS:

The table 1 presented the blood pressure results, where we observed that the SBP levels was significant increased (P<0.01) in chewers group when we compared to control one. Also, the level of DBP was found elevate in the concerning group (P<0.05).

Table 1: Meanof systolic blood pressures (SBP) and diastolic blood pressures (DBP) in tobacco chewers and controls groups

Blood pressure	Controls	Chewers
SBP (mmHg)	11.79±0.283	12.718±0.313^**
DBP (mmHg)	7.73±0.295	8.327±0.284^*

Values are mean ± SEM (n=11). * p<0.05 and ** p<0.01: significantly different compared to the control group.

Our obtained results show that there was a significant elevation (p<0.001) in total cholesterol (TC), triglycerides (TG) and VLDL-c levels, additionally to LDL-c level (p<0.01) in chewers group when we compared to control group. However, there are non-significant variations in HDL-c level (Table 02).

Table 02: Meanlipid profile levels in tobacco chewer and controlsgroups

parameters	Controls	Chewers
Serum TC (g/l)	1.635± 0.081	2.068±0.118^***
Serum TG (g/l)	0.758±0.072	1.345±0.133^***
Serum HDL-c (g/l)	0.526±0.019	0.504±0.013
Serum LDL-c (g/l)	0.969±0.070	1.251±0.092^**
Serum VLDL-c (g/l)	0.154±0.016	0.268±0.026^***

Values are mean ± SEM (n=11). ** p<0.01 and *** p<0.001: significantly different compared to the control group.

On comparisonwith controls, the atherogenic index (AI) of chewers were found to be statistically significant elevated (p<0.01) (Figure 01).

Figure 1: Variation of the mean atherogenic index (AI) in tobacco chewers and controls groups. Values are mean ± SEM (n=11). ** p<0.01: significantly different compared to the control group.

From table 3, we noticed a non-significance change (p >0.05) in the blood sugar, AST, serum urea and creatinine levels chewers compared to control.

Table 3: Mean serum biochemical parameters in tobacco chewers and controlsgroups

Parameters	Controls	Chewers
Serum Blood glucose (g/l)	0.911±0.0299	0.965±0.05
Serum Urea(g/l)	0.1945±0.0099	0.2017±0.0145
Serum Creatinine (mg/l)	9.385±0.789	10.266±0.449
Serum AST(UI)	23.64±1.61	21.44±1.20

Values are mean ± SEM (n=11).

Our results in table 04 showed that the level of RBC, Hgb, HTC are significantly decreased (p<0.001) while significant increase of PLT level (p<0.05) in tobacco chewers compared to the controls. Concerning the leukocyte line, the results showed a non-significantchange (p >0.05) in WBC and Lym levels in chewers group compered to controls one.

Table 4: Erythrocyte and Leukocyte line in tobacco chewers and controls groups

Parameters	Controls	Chewers
Red blood cell (10⁶/µl)	5.255±0.153	4.6136±0.07^***
Hemoglobin (g/dl)	14.440±0.316	13.027±0.24^***
Hematocrit (%)	44.86±1.28	39.553±0.952^***
Mean Corpuscular Volume (FL)	85.68±2.12	85.55±1.35
Platelet (10³/µl)	203.6±11.7	224.75±8.55^*
White blood cell (10³/µl)	6.091±0.294	6.093±0.296
Lymphocytes (10³/µl)	2.139±0.181	2.205±0.157

Values are mean ± SEM (n=11). *p<0.05, **p<0.01 and ***p<0.001: significantly different compared to the control group.

DISCUSSION:

The present study was undertaken to study the effects of habitual consumption of tobacco chewing on various hematological and biochemical parameters in Algerian men. Tobacco contains various substances which are carcinogens, co-carcinogens, mutagen, toxins, antigens and pharmacological active agents [17]. Nicotine is an alkaloid that occurs in highest concentrations in leaves of the tobacco plant. Approximately 95% of the alkaloid content of tobacco is nicotine [18]. Smokeless tobacco is not burned, but is placed in the mouth, and sometimes contains flavorings. They come in the form of moist, dry, or single-use pouches and are placed between the lip and cheek, or are inhaled through the nose [19]. From our results, we showed the increase of lipid profile on chewers due to the great absorption dose of nicotine from smokeless tobacco [20]. The nicotine is the active ingredient in tobacco [21]. Which stimulates sympathetic adrenal system leading to increase secretion of catecholamine’s which increase the lipolysis in humans [22], via activation of adenylyl cyclase, these increased free fatty acids in liver give rise to increased hepatic triglyceride, VLDL-c synthesis [23], LDL-c and lowered HDL-c [24]. thus increasing the concentration of triglyceride, total cholesterol, VLDL-cand LDL-c in blood. The increase in these parameters increases the likelihood of developing cardiovascular diseases [25].

The mean values of atherogenic indice AI was significantly increasedon chewers group this results are in accordance with studies by Gadpal et al (2015) [26]. Therefore, the augment of total cholesterol makes the increase of atherogenic indice, which may be predicting cardiovascular risk in various clinical settings [27]. Tobacco has been recognized as a major risk factor for the development of ischaemic heart disease [28]. Systolic as well as diastolic blood pressure was greater in tobacco consuming groups, due to the sympathicoadrenal-activating properties of nicotine and their acute effects in system cardiovascular [29]. Although the diastolic blood pressure was significantly greater in tobacco chewers this could be due to high Na+ content in smokeless tobacco [30] and a more prolonged absorption of tobacco when chewed accompanied with more prolonged vasoconstriction [31].

Sharif et al (2014) confirmed that the nicotine inhibits the function of erythrocytes and fibroblasts and causes the diminished proliferation of red blood cells, which explain the decrease of RBCs count in chewers [32]. In the present study, The HgB and HCT levels was found to be significantly lower in chewers group as compared to the controls, this may be reflecting to nicotine effect on these parameters as what was present in study of Singh and Singh (2019) [33]. A decrease in RBC and hemoglobin necessarily leads to anemia disease [34]. The previous reports have shown that chronic use of nicotine causes platelet activation, which increased their count in blood [35].

CONCLUSION:

We conclude that the alteration in lipid profile and blood pressure is clearly determined for the chewer’s subject. So, the tobacco chewing is carry equal cardiovascular risk as far as alterations in lipid profile and blood pressure. Thus, any change in the body will reflect immediately in lipid continents of the biological system. Also, tobacco chewing is responsible on appearance of anemia symptoms.

ACKNOWLEDGEMENTS:

We would like to thank the Faculty of Sciences of Nature and Life, University of El Oued, Algeria for the permission to utilize the facilities to make this work.

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Received on 09.09.2020 Modified on 28.09.2020

Res. J. Pharmacology and Pharmacodynamics.2021; 13(1):1-4.

DOI: 10.5958/2321-5836.2021.00001.X