Effects of noise exposure on catalase activity of growing lymphocytes (original) (raw)
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Open Access Library Journal, 2021
This is a detailed experimental and comparative study evaluating the harmful effects of graded loud noise on hematological and antioxidant in Wistar albino rats. Wistar albino rats were divided into a control group (those kept away from the noise due to a generator set), groups 1 (exposed to varied, 85 - 105 db levels of loud noise from a generator) and groups 2 (exposed to less, 40 - 55 db levels of loud noise from generator set) and exposed to way off fumes from electrical generator sounds at different sound level for 8 hours each day for 28 days. The result indicated that activities and concentrations of the antioxidant enzymes: glutathione peroxidase, catalase and glutathione increased significantly (p < 0.05) when compared with the control group in group 1. There was also an increase in the concentrations of malondialdehyde and hematological parameters (RBC, WBC, PCV, hemoglobin, platelets) among the rats exposed to loud noise from a generator set in group 2, when compared t...
The effects of noise stress on leukocyte function in rats
Research in nursing & …, 2007
It has been reported that exposure to increased noise levels impairs wound healing in surgical patients and in rats. The purpose of the present study was to determine if exposure to noise stress would alter the biological function of neutrophils, macrophages, and lymphocytes, leukocytes that are involved in wound healing. Rats were exposed to 80 db of "rock" music for 24 hr, during which time the control animals were maintained in their usual environment. Leukocyte subpopulations were obtained and stimulated in vitro. Neutrophils and macrophages from noise-exposed animals secreted significantly less superoxide anion and interleukin-1 than cells from control animals. Lymphocyte function was not altered following noise stress. We conclude that short-term exposure of rats to noise stress alters some of the biological functions of leukocytes.
Influence of noise exposure on antioxidant system and TEOAEs in rabbits
European Archives of Oto-Rhino-Laryngology, 2001
Noise exposure may cause hearing loss. The precise mechanism leading to cochlear damage in acoustic trauma is not known. Eight rabbits were used in this study. Transient evoked otoacoustic emissions (TEOAEs) were recorded in all animals and blood malondialdehyde (MDA) and glutathione (GSH) levels were determined. All rabbits were then exposed to 100 dB SPL broadband noise for 1 h. TEOAEs were recorded again and blood MDA and GSH levels determined following noise exposure. The reproducibility scores of the TEOAE measurements were found to be significantly lower (P < 0.01), whereas the amplitudes and signal-to-noise values of emissions decreased (P > 0.01) in rabbits exposed to noise. The TEOAE energies were poor at 4 kHz. During this threshold shift, GSH blood levels decreased and MDA levels increased, indicating that there is a close relationship between noise-induced hearing loss and the antioxidant system. These findings indicate that TEOAE recording is an excellent test for detecting effects of noise on hearing.
The effects of industrial noise exposure on lipid peroxidation and antioxidant enzymes among workers
International Archives of Occupational and Environmental Health, 2019
The aim of this study was to measure individual exposure to noise and its effect on the levels of lipid peroxidation and enzymatic antioxidant defense. Methods In this cross-sectional study, 94 male workers working in a food factory in Shahroud, Iran, were selected as the case group and 112 people were also included as the control group. The level of exposure to noise was measured using a dosimeter and the equivalent level was calculated. The levels of malondialdehyde (MDA), catalase (Cat), superoxide dismutase (SOD), and Total Antioxidant Capacity (TAC) were measured in the serum samples of all participants. Independent t test, one-way ANOVA, and multivariate linear regression were used to analyze the data. Results The levels of MDA, Cat, and TAC were significantly higher in staff exposed to noise than in the controls. The starch and warehouse units' staff were exposed to the highest (99.3 ± 3.23 dB) and lowest (77.1 ± 9.68 dB) mean levels of sound pressure. Based on the linear regression model, noise exposure level was the most important predictor variable for levels of MDA (β = 0.48, CI 95% = 0.04-0.93), Cat (β = 0.43, CI 95% = 0.05-0.83), and TAC (β = 0.11, CI 95% = 0.06-0.16). Conclusions Noise exposure increases the production of free radicals. As exposure rate increases, the levels of MDA, Cat, and TAC enzymes increase as well.
The Laryngoscope, 2004
The objective was to investigate the effects of both noise exposure and ascorbic acid on oxidative status and hearing thresholds of rabbits. Study Design: Randomized prospective animal study comparing oxidative parameters and otoacoustic emissions in two rabbit groups exposed to noise. One group was given absorbic acid, the other group was not given any treatment. Methods: Two groups of rabbits were used in the study; each group had six rabbits. The six rabbits in the first group were not given any treatment, whereas 500 mg intramuscular ascorbic acid twice daily for 2 1 ⁄2 days was given to the six rabbits in the second group. Transient evoked otoacoustic emissions were recorded in all animals before and after noise exposure. Total protein sulfhydryl groups, carbonyl contents, and malondialdehyde levels, as well as erythrocyte glutathione, superoxide dismutase, and catalase enzyme levels, were measured in all rabbits. All the rabbits were exposed to noise (100 dB sound pressure level, 1000 Hz, 1 h), and transient evoked otoacoustic emissions were recorded again. Results: When oxidative parameters before noise exposure were compared, erythrocyte glutathione and catalase enzyme levels were detected to be higher in the second group (P < .05). In the first group of rabbits after noise exposure, total protein sulfhydryl groups were found to be reduced (P < .05), whereas plasma carbonyl contents and malondialdehyde levels were elevated significantly (P < .05). In this group, erythrocyte glutathione, superoxide dismutase, and catalase enzyme levels were low (P < .05). In the second group, which was given ascorbic acid, total protein sulfhydryl groups were reduced (P < .05), whereas plasma carbonyl contents and malondialdehyde levels did not change (P > .05) following noise exposure. In the second group, erythrocyte glu-tathione and catalase enzyme levels were reduced (P < .05), but superoxide dismutase levels did not change (P > .05). Transient evoked otoacoustic emissions after noise exposure were weak in both groups, but reproducibility and signal-to-noise ratios were higher in the second group (P < .05). Conclusion: Ascorbic acid treatment inhibited both lipid peroxidation and oxidative damage of proteins in rabbits exposed to noise. The study data suggest, at least, that oxidative status should be included in the physiopathology of noise-induced hearing loss; in addition, a brief application of ascorbic acid before noise exposure appeared to play a protective role for cochlea.
Time-dependent differential changes of immune function in rats exposed to chronic intermittent noise
Physiology & behavior, 1996
Noise is a highly relevant environmental and clinical stressor. Compared to most other experimental stressors, noise is a modest activator of neuroendocrine pathways that mimic the situation in human health where neuroendocrine activation by environmental stressors is often absent or difficult to establish. Little is known about the effects of noise exposure on the immune system. In the present work, the effects of a low-intensity chronic intermittent unpredictable noise regimen on various parameters of immune function was studied. Male wistar rats were exposed to a randomized noise protocol (white noise, 85 dB, 2-20 kHz) for 10 h per day, 15 min per h over a total period of 3 weeks. Control animals were exposed to ambient sound only. Immune function was monitored after 24 h, 7 days, and 21 days of noise exposure. Noise induced several significant changes in immune function in a time-dependent differential pattern involving both immunosuppression and immunoenhancement. After 24 h, s...
Free Radical Research, 2020
Background: Large epidemiological studies point towards a link between the incidence of arterial hypertension, ischaemic heart disease, metabolic disease and exposure to traffic noise, supporting the role of noise exposure as an independent cardiovascular risk factor. We characterised the underlying molecular mechanisms leading to noise-dependent adverse effects on the vasculature and myocardium in an animal model of aircraft noise exposure and identified oxidative stress and inflammation as central players in mediating vascular and cardiac dysfunction. Here, we studied the impact of noise-induced oxidative DNA damage on vascular function in DNArepair deficient 8-oxoguanine glycosylase knockout (Ogg1-/-) mice. Methods and results: Noise exposure (peak sound levels of 85 and mean sound level of 72 dB(A) applied for 4d) caused oxidative DNA damage (8-oxoguanine) and enhanced NOX-2 expression in C57BL/6 mice with synergistic increases in Ogg1-/mice (shown by immunohistochemistry). A similar pattern was found for oxidative burst of blood leukocytes and other markers of oxidative stress (4-hydroxynonenal, 3-nitrotyrosine) and inflammation (cyclooxygenase-2). We observed additive impairment of noise exposure and genetic Ogg1 deficiency on endotheliumindependent relaxation (nitroglycerine), which may be due to exacerbated oxidative DNA damage leading to leukocyte activation and oxidative aldehyde dehydrogenase inhibition. Conclusions: The finding that chronic noise exposure causes oxidative DNA damage in mice is worrisome since these potential mutagenic lesions could contribute to cancer progression. Human field studies have to demonstrate whether oxidative DNA damage is also found in urban populations with high levels of noise exposure as recently shown for workers with high occupational noise exposure.