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Research Article | Volume 14 Issue: 4 (Jul-Aug, 2024) | Pages 751 - 756
Impact of Oxidative Stress on Brainstem Auditory Evoked Potentials (BAEP) in Tobacco Smokers: A Comprehensive Analysis
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1
Assistant Professor, Physiology, Career Institute of Medical Sciences, Lucknow. U.P. India
2
Assistant Professor, Biochemistry, Career Institute of Medical Sciences, Lucknow. U.P. India
3
Assistant Professor, Physiology, AIIMS, Patna, Bihar. India
4
Assistant Professor, Physiology, T.S. Misra Medical College & Hospital, Lucknow. India
5
Assistant Professor, Physiology, Mahamaya Rajkiya Allopathic Medical College, Ambedkar Nagar, U.P. India
6
Professor, Physiology, National Institute of Medical Sciences & Research, Jaipur, Rajasthan, India
7
Associate Professor, Physiology, Career Institute of Medical Sciences, Lucknow. U.P. India
Under a Creative Commons license
Open Access
Received
June 28, 2024
Revised
July 25, 2024
Accepted
Aug. 2, 2024
Published
Aug. 21, 2024
Abstract

According to the World Health Organization (WHO), the global tobacco epidemic stands as one of the most significant threats to public health in history. With a staggering death toll exceeding 8 million annually, the impact is profound. Smoking prevalence varies greatly between regions and even within countries of the same region. Currently, the highest rates of male smoking are observed in the Western Pacific nations. In India, tobacco usage, encompassing both smoking and non-smoking forms, remains prevalent. Smoking cigarettes is recognized as a major contributor to various neurological disorders, with oxidative stress implicated as a potential mechanism of smoking-related harm resulting brainstem hypoxia which contributes to abnormalities in brainstem auditory evoked potentials (BAEP), resulting in significant impairment of the functions of the eighth cranial nerve and the brainstem among smokers. This research investigates the profound effects of oxidative stress on brainstem auditory evoked potentials (BAEP), in tobacco smokers. The study encompasses a diverse array of measurements, including anthropometric data, blood pressure, brainstem auditory evoked potentials (BAEP) oxidative stress markers (malondialdehyde - MDA and superoxide dismutase - SOD), and serum electrolytes. The results shed light on the intricate relationship between tobacco smoking, oxidative stress, and neurological outcomes.

Keywords
INTRODUCTION

According to the WHO, the tobacco epidemic is one of the greatest public health threats the world has ever faced. The death rate in the world is more than 8 million per year. More than 7 million of these deaths are due to direct tobacco use, and approximately 1.2 million are due to nonsmokers exposed to indirect smoking. Tobacco smoking is the most common form of tobacco consumption in the world. Other tobacco products include water pipe tobacco, various smokeless tobacco products, cigars, cigarillos, pipe tobacco, bidis etc. 1 Natives began using tobacco for pipes, cigars, and snuffs when Columbus and his successors recorded tobacco in other countries. As a result, Portuguese and Spanish sailors helped spread different types of tobacco for use around the world.4 Smoking is a major risk factor in the development of COPD and COPD-related peripheral neuropathy. 9 Grünberg Schaefer hypothesized the mechanism of why stress is associated with increased smoking. (a) Smoking reduces stress levels due to nicotine or other chemicals in tobacco reduces some aspects of stress.  (b)  Stress reduces the effects of nicotine, thereby Increasing the self- administration of nicotine, Stress-free situation; (c) Stress reduces the availability of nicotine, which leads to failure Withdrawal and consequent increase in tobacco consumption. (d) Smoking cigarettes (and Nicotine) Improves cognitive function affected by the harmful effects of stress Understanding. 13 Brainstem hypoxia, associated with COPD leads to the brainstem auditory evoked potential (BAEP) abnormalities, the functions of the eighth cranial nerve and brainstem were highly impaired in severe COPD.21 Smoking not only produces reactive oxygen radicals in smoke, but can also increase oxidative stress by weakening antioxidant defense systems. 28 Chronic smoking not only slows down the conduction velocity of sensory nerves, but also leads to oxidative stress in smokers. This effect is due to the reduction of total antioxidants in plasma volume. Oxidative stress can occur in smokers with impaired tobacco nerve conduction. 2

 

This study aims to observe the effect of oxidative stress on Brainstem Auditory Evoked Potential (BAEP) & to determine the status of oxidative stress in smokers and non-smokers.

MATERIAL & METHODS

The study was conducted in the Department of Physiology with collaboration department of Biochemistry of Career Institute of Medical Sciences & Hospital, Lucknow, Uttar Pradesh with intellectual assistance from Nims University Rajasthan, Jaipur. after obtaining ethical approval from the National Institute of Medical Sciences and Research, Nims University Rajasthan, Jaipur and also from Institutional Ethical Committee Career Institute of Medical Sciences and Hospital, Lucknow

 

This was a cross-sectional study. In this study, we recruited 100 adult males, who have been smoking tobacco for the last 5 years (≥2 pack years)133 with the age group of 25-55 years as Cases and age-matched 100 nonsmokers were also recruited after explaining the aim,

 

objectives and significance of the study, written informed consent is also taken. Anthropometric data, including age, height, weight, and BMI, were measured.

 

The Brainstem Auditory Evoked Potential (BAEP) testing was conducted in the Research Laboratory of the Department of Physiology at CIMS&H, utilizing the NEURO-STIM software (Medicaid system, Chandigarh, India), with default settings. Patients were positioned lying down, ensuring a relaxed and comfortable state, crucial for accurately detecting hearing thresholds during BAEP assessment. A cushion or pillow was placed beneath the neck to enhance patient comfort. The testing environment was maintained in a quiet condition, minimizing extraneous noise to facilitate optimal concentration on the test stimuli and masking noise. Electrode placement adhered to the International 10/20 System, utilizing a single-channel configuration. Electrode sites were cleansed with an abrasive cleanser or spirit before application. Conductive paste was then applied to the surface electrodes, positioned over the mastoid or ear (A1, A2) bilaterally, as well as on the forehead (Fz) and vertex (Cz). Monaural delivery of alternate (condensation and rarefaction) clicks through headphones occurred at a repetition rate of 11.1 clicks per second, with a stimulus intensity set at 80 dB (decibels). Both ipsilateral (Ai) and contralateral (Ac) ears of each subject were tested, with at least two recording trials conducted for each ear. A total of 2000 responses were averaged for each recording. Subsequently, brainstem auditory evoked potentials were recorded and analyzed. The identification of waves, including waves I, II, III, IV, and V was performed based on their standard characteristics.

 

Serum Malondialdehyde (MDA) was estimated from serum was done by a sensitive spectrophotometric method described by Buege et al. in 1978143. MDA in the catabolite of lipid peroxide can react with thiobarbituric acid (TBA) and produce red compound, which has a maximum absorption peak at 532 nm.

 

Serum Superoxide Dismutase (SOD) was estimated by using the Superoxide Dismutase Activity kit. All samples should be read off of the standard curve, which was created using a bovine erythrocyte SOD standard that was provided. In our uniquely coloured sample diluent, samples are diluted before being added to the wells.

 

The Xanthine Oxidase Reagent

is added after the substrate, and the mixture is then left to sit at room temperature for 20 minutes. In the presence of oxygen, the enzyme xanthine oxidase produces superoxide, which changes a colourless substrate in the detection reagent into a yellow-coloured product. At 450 nm, the coloured product is read. Superoxide levels drop and the amount of yellow product decreases as SOD levels rise in the samples.

STATISTICAL ANALYSIS

Results were analyzed by using SPSS 29 Software.

Unpaired T-test was applied to analyze the statistical significance of changes in the BAEP and biochemical parameters. Pearson correlation was used to show the correction of oxidative stress with BAEP waves. p value <0.05 was taken as statistically significant.

Observation Table 1

Parameters

Non-smokers (n=100)

Smokers (n=100)

t-value

p-value

Age (mean± SD) (years)

36.16 ±7.81

37.96 ±8.7

1.59

0.11

Height (m.)

1.64±0.09

1.68±0.05

3.89

0.0001

Weight (Kg.)

60.79±10.65

70.75±10.10

6.79

0.58

BMI (Kg/m2)

22.63±4.09

25.12±3.60

4.57

0.09

 

 

The two-tailed P value is more than 0.05 in the ages of case and control groups. By conventional criteria, this difference is considered to be (p-value =0.11) and (t-value =1.59).

 

Total of 200 subjects were included in this study of which 100 cases (tobacco smokers) and 100 controls (non-smokers) Average age for the cases was 37.96 ±8.70 years and an average age of the control were 36.16 ±7.81 years and found statistically significant (p<0.05) Body Mass Index of cases (22.63±4.09) and of control subjects (25.12±3.60) was not found statistically significant (p<0.05)

Table 2

Parameter

Cases

Controls

t-value

p-value

S. B.P (mm Hg.)

133.76±5.58

126.39±10.89

6.02

0.0001

D. B.P. (mm Hg.)

81.52±5.00

77.10±6.13

5.59

0.0001

A. Pulse(beats/min)

79. 44±9.26

8019±9.03

0.58

0.281

 

 

Descriptive Statistics for components of Blood Pressure and Arterial Pulse were described in Table 3. Systolic Blood pressure was observed to be significantly more (p<0.001) in cases (133.76±5.58 mm Hg) than control subjects (126.39±10.89 mmHg). Diastolic Blood pressure was observed to be significantly more (p<0.001) in cases (81.52±5.00mm Hg) than control subjects (77.10±6.13mmHg). No significant difference observed for the Arterial Pulse of cases (79.44±9.26) and control (80.19±9.03beats/min) with a p = 0.273.

 

Brainstem Auditory Evoked Potential (BAEP)

Brainstem Auditory Evoked Potential (BAEP) was observed in the control & case

groups with a sound intensity between 80 dB, and a comparison of the right and left ear was done separately.

 

Table 3. Right Ear Latencies and interpeak latencies between study groups

Parameter Latencies and interpeak Latencies (msec.)

Cases

Controls

t-value

p-value

Wave I

 

1.66±0.07

 

 

1.54±0.02

 

 

16.48

 

 

0.0001

 

Wave II

 

2.84±0.11

 

 

2.66±0.07

 

 

13.81

 

 

0.0001

 

Wave III

 

3.87±0.13

 

 

3.64±0.08

 

 

15.07

 

 

0.0001

 

Wave IV

 

4.98±0.19

 

 

4.92±0.20

 

 

2.18

 

 

0.031

 

Wave V

5.83±0.13

5.66±0.09

10.75

0.0001

IPL I-III

2.21±0.16

2.10±0.08

6.15

0.0001

IPL-III-V

1.96±0.20

2.03±0.12

3.00

0.003

IPL-I-V

4.17±0.14

4.14±0.09

 

1.8025

 

0.0001

                                   

 

Latencies (msec.) of BAEP (Right Ear) wave I (1.66±0.07), II (2.84±0.11), III (3.87±0.13) and wave V (5.83±0.13) was significantly higher in tobacco smokers as compared to non-smokers wave I (1.54±0.02), II (2.66±0.07), III (3.64±0.08) and wave V (5.66±0.09). While wave IV (4.98±0.19) of BAEP of the case when compared with control (wave IV 4.92±0.20) did not show any statistically significance. Interpeak latencies (msec.) of Brainstem Auditory Evoked Potential (Right ear) IPL IIII (2.21±0.16), I IPL III-V (1.96±0.20), IPL I-V (4.17±0.14) was significantly higher in tobacco smokers as compared to Interpeak latencies of non-smokers IPL I-III (2.10±0.08), I IPL III-V (2.03±0.12), IPL I-V (4.14±0.09).

 

 

 

Table 4 Left Ear Latencies and interpeak latencies between study groups

Parameter Latencies and interpeak Latencies (msec.)

Cases

Controls

t-value

p-value

Wave I

1.66±0.07

1.55±0.01

15.56

0.0001

Wave II

2.84±0.10

2.67±0.07

13.93

0.0001

Wave III

3.88±0.13

3.62±0.07

17.61

0.0001

Wave IV

4.97±0.19

4.92±0.19

1.86

0.064

Wave V

5.83±0.14

5.66±0.10

9.89

0.0001

IPL I-III

2.22±0.16

2.08±0.08

29.00

0.0001

IPL-III-V

1.95±0.21

2.04±0.12

3.72

0.003

IPL-I-V

4.17±0.14

4.11±0.10

3.49

0.0730

 

 

 

The two-tailed pvalue is less than 0.0001 in wave I, II, III and V between case and control groups. According to normal standards, this variation is to be extremely statistically significant. While no such statistically significant found in wave IV between case and control groups. The two-tailed pvalue is less than 0.05 in all three Interpeak Latencies (I- II, III-V and I-V) between case and control groups. According to normal standards, this variation is to be extremely statistically significant.

 

Table 5. Correlation of MDA with BAEP waves & with Interpeak Latencies (Right Ear) in tobacco smokers.

Values

Wave I

Wave II

Wave III

Wave IV

Wave V

IPL I-III

IPL-III-V

IPL I-V

r

0.11

-0.08

0.10

-0.10

0.07

0.03

-0.02

0.01

P

0.28

0.44

0.32

0.32

0.48

0.77

0.83

0.94

 

This table shows the correlation between MDA with BAEP waves latencies of Right Ear. Negative correlation of MDA with BAEP waves latencies II & IV were found. Positive correlation of MDA with BAEP waves latencies I, III & V were found. But no statistically significant found between MDA and BAEP waves latencies a pvalue>0.05. This table also shows the correlation between MDA with BAEP waves Interpeak latencies of left Ear. Negative correlation found with IPL III-V and positive correlation of MDA with IPL I- III and I-V, but no statistically significance was found.

 

Table 6. Correlation of MDA with BAEP waves & with Interpeak Latencies (Left Ear) in tobacco smokers.

Values

Wave I

Wave II

Wave III

Wave IV

Wave V

IPL I-III

IPL-III-V

IPL I-V

r

0.06

-0.08

0.07

-0.11

0.06

0.03

-0.01

0.02

p

0.52

0.44

0.48

0.30

0.58

0.77

0.94

0.83

 

This table shows the correlation between MDA with BAEP waves latencies of left Ear. Negative correlation of MDA with BAEP waves latencies II & IV were found. Positive correlation of MDA with BAEP waves latencies I, III & V were found. But no statistically significant found between MDA and BAEP waves latencies a pvalue>0.05. This table also shows the correlation between MDA with BAEP waves Interpeak latencies of left Ear. Negative correlation found with IPL III-V and positive correlation of MDA with IPL I- III and I-V, but no statistically significance was found.

 

Table 07. Correlation of SOD with BAEP waves (Right Ear) in tobacco smokers.

Values

Wave I

Wave II

Wave III

Wave IV

Wave V

IPL I-III

IPL-III-V

IPL I-V

r

-0.06

-0.05

-0.04

-0.10

-0.15

-0.01

-0.12

-0.17

p

0.54

0.62

0.68

0.32

0.03

0.95

0.25

0.08

 

This table shows the correlation between SOD with BAEP waves latencies of Right Ear. Negative correlation found with all waves (I, II, III, IV and V). But no statistically significant found between SOD and BAEP waves latencies as pvalue>0.05. This table also shows the correlation between SOD with Interpeak latencies. Negative correlation found with all IPL I-III, IPL III-V and IPL I-V. But no statistically significant found between SOD and BAEP waves Interpeak latencies as pvalue>0.05

 

Table 08. Correlation of SOD with BAEP waves (Left Ear) in tobacco smokers.

Values

Wave I

Wave II

Wave III

Wave IV

Wave V

IPL I-III

IPL-III-V

IPL I-V

r

-0.08

-0.04

-0.03

-0.01

-0.18

0.01

-0.10

-0.14

p

0.44

0.68

0.74

0.89

0.07

0.93

0.31

0.17

 

This table shows the correlation between SOD with BAEP waves latencies of left Ear. Negative correlation of SOD with BAEP waves latencies I, II III, V and IV were found. But no statistically significant found between SOD and BAEP waves latencies a pvalue>0.05. This table also shows the correlation between SOD with BAEP waves Interpeak latencies of left Ear. Positive correlation found with IPL I- III and negative correlation of SOD with IPL III-V and I-V were found.

 

Table 09. Correlation of MDA with SOD in tobacco smokers

Values

SOD

R

-0.051

p

0.66

 

This table shows the correlation between MDA with SOD Negative correlation of MDA with SOD was found. But statistically not significant as pvalue >0.05

 

Correlation with Oxidative Stress Markers:

Correlation analyses with oxidative stress markers (MDA and SOD) demonstrated intricate relationships with BAEP and interpeak latencies. MDA showed negative correlations with certain BAEP waves, while SOD displayed complex associations, emphasizing the need for further exploration.

DISCUSSION

Smoking is known to have detrimental effects on health, including increasing the risk of cardiovascular diseases, respiratory illnesses, and various cancers. Additionally, smoking can also impact hearing health, potentially leading to conditions such as hearing loss. Studies have investigated the effects of smoking on auditory function using Brainstem Auditory Evoked Potentials (BAEP) testing, which assesses the electrical activity of the auditory system at the brainstem level. Martins DMT (2016) 23 explains that BAEP testing allows mapping of auditory pathways and assessment of auditory system activity. Recent Belgian studies provide evidence that smoking exacerbates high-frequency hearing loss. In this present study, comparison of WAVE- I, II, III, IV, V and Inter-Peak Latencies (IPL) I-III, III-V and I-V was done between the tobacco smokers (100) and non- smokers (100) groups bilaterally. When we compare the Latencies of bilateral BAEP shows statistically significant prolongation of Latencies of Wave-I, II, III, V and Inter-Peak Latencies (IPL) I-III, III- V I-V of Case Group to Control Group. Whereas only Wave-IV, does not found significant difference, between cases group and control group. Similar findings were reported by Waseem SMA et al. (2018) 60 found significant differences in Brainstem Auditory Evoked Potentials (BAEP) between smokers with Chronic Obstructive Pulmonary Disease (COPD) and non-smokers. Specifically, significant differences were observed in Waves III, IV, and V, as well as Inter-Peak latencies (IPL) I-V, in both the right and left ears. However, no significant differences were found in Wave I and Wave II between non-smokers and smokers without COPD, indicating that the effects on auditory function may be specific to smokers with COPD. In their study, Abhinav Dixit et al. (2019) 126 demonstrated a significant increase in the latencies of waves I and II in individuals in an acute smoking state compared to non-smokers. However, no significant changes were observed in the latencies of other waves or in interpeak latencies. Similarly, Harkrider et al. (2001) 127 investigated the effects of nicotine patches on BAEP in non-smokers and found significant changes in the amplitude and latency of wave

  1. This study differed from others by using nicotine patches to assess BAEP effects in non-smokers. In contrast, Knott VJ (1987) 128 found no differences in latency or amplitudes of waves I and III between acute and chronic smoking states.
CONCLUSION

This comprehensive study elucidates the multifaceted impact of oxidative stress induced by tobacco smoking on neurophysiological parameters. The findings underscore the need for targeted interventions to mitigate the adverse neurological effects associated with smoking. Further research is essential to unravel the intricacies of these relationships and inform public health strategies aimed at reducing the burden of tobacco-related neurological disorders.

 

LIMITATIONS:

Limitation of this study is less sample size, only 100 subjects were selected which is very less in numbers as compared to prevalence of tobacco smoking. Female subjects are not included in this study, due to social sigma.

 

Since our study was based on willingness of participants for the assessment of BAEP & oxidative Stress due to logistic difficulties, a randomized controlled study further exploring our aims is highly recommended on larger populations of different region world-wide, to get wider data for standardization.

 

Conflict of Interest: Nil

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