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| Year : 2014
| Volume
: 16 | Issue : 71 | Page
: 213-217 |
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| Effects of high frequency noise on female rat's multi-organ histology |
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Laijun Xue1, Dajun Zhang1, Xiaokaiti·Yibulayin2, Ting Wang3, Xi Shou4
1 Department of Occupational Diseases, Xinjiang Karamay Municipal Center Hospital, Karamay, Xinjiang, China
2 Department of Occupational Health and Environmental Health, School of Public Health, Xinjiang Medical University, Urumqi, Xinjiang, China
3 Science and Technology Information Department, Xinjiang Medical University Library, Urumqi, Xinjiang, China
4 Department of Animal Models, Animal Research Section of Clinical Medical Research College, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China
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| Date of Web Publication | 18-Jul-2014 |
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To investigate the pathological damage of high-frequency stable noise exposure on the brain, heart, liver, and spleen of female rat's. Controlled animal intervention study. Twenty female Sprague-Dawley rats were randomly divided into experimental and control groups with 10 rats in each group. Rats in the experimental group were exposed to continuous high-frequency stable noise for 2 weeks (3 h/day)followed by the pathological damages in the rat's brain, heart, liver, and spleen were compared with those of the control group. After 2 weeks' continuous exposure to high-frequency stable noise, compared with the control group, the most prominent histopathologic changes in the brain tissue structures of the experimental group included loose disorder, hyperemia, edema, blood vessels expand, glial cell hyperplasia, mild atypia in some areas (hyperchromatic nuclei, irregular karyotype), and no degeneration and necrosis. There were dilatation and congestion of central vein, hepatic sinus, and interlobular veins of liver tissue. The structure of hepatic lobule was destroyed by inflammatory cell infiltration, as well as lymphoid nodule formation. There was hyperemia in spleen, but the structure was clear. There was extravasated blood, and the splenic sinuses were highly expanded by a blood clot. Hyperplasias of the lymphoid of white pulp were also active. There was dilation and congestion in myocardial interstitial vascular, and there was mild degeneration and hyperemia in myocardial cells. No hemorrhage and myocardial necrosis were observed. High-frequency stable noise can cause pathological damage in brain, liver, spleen, and heart tissues of female rat at a various degree. Keywords: Female rats, noise, the pathological injury of viscera
How to cite this article:
Xue L, Zhang D, Xiaokaiti·Yibulayin, Wang T, Shou X. Effects of high frequency noise on female rat's multi-organ histology. Noise Health 2014;16:213-7 |
| Introduction | |  |
In the modern urban societies, noise is a well-recognized environmental hazard. In the last three decades, most of these nonauditory effects of noise were related to the systemic effects of high frequency noise, which could lead to neurologic, [1] vascular, [2] immune, [3] and cardiac disorders. [4] Noise may also cause health disorders through annoyance and stress, such as oxidative stress. Statistics from Ersoy et al. study in the Turkey [5] showed that brain tissue was affected by oxidative stress as a result of continued exposure to noise. Furthermore, several epidemiologic studies [6],[7] have also reported that chronic noise exposure significantly increased blood pressure during working and sleeping periods. The exposure to chronic noise may affect the immune system, [8] too. Based on the Pascuan study, [9] noise exposure induced a decrease in corticosterone and catecholamines levels in BALB/c mice, which could seriously affect immune responses in susceptible individuals. In addition, studies of some other fields [10],[11],[12] have demonstrated that noise can increases collagen I and III in the extracellular matrix and induces ultrastructural alterations in the cardiomyocytes. Thus in this study, we conducted experiments to further evaluate the effect of noise on brain, heart, liver, and spleen by using experimental rats.
| Methods | | |
Randomization and treatment
We used 20 adult (weight about 200 g) female Sprague-Dawley (SD) rats that were purchased from a Xinjiang Animal Experimental Center (2011-0001) and fed in Animal Research Section of Clinical Medical Research College in Xinjiang Medical University. Twenty female SD rats were randomly divided into the experimental and control groups with 10 rats in each group. The rats were first kept for 1 week in the general animal house of Xinjiang Key Laboratory for medical animal model research (through the animal experiment of Association for Assessment and Accreditation of Laboratory Animal Care international certification), where the room temperature was set at 24-25°C. The rats had unrestricted access to food (commercial chow) and water. Rats in the experimental group were then transferred to a noise-insulated special animal room equipped with the noise-generating device, and they were kept for 2 weeks (3 h/day). The project was approved by the Medical Ethics Committee of Xinjiang Medical University. All staff involved in the experiment were trained and assessed to ensure their qualification. Animal breeding and experiments were performed in line with the "quality management approach to laboratory animals," and all efforts were made to minimize the number of animals used and their suffering.
Noise exposure
We continuously recorded electric audiometer acoustic for 30 min and reproduced it in a sound-insulated animal's room. The high frequency noise is similar to noise of a steam turbine or a generator room from the large thermal power plant of Karamay. The exposure noise level was adjusted to 95 dB(A). The intensity of 95 dB(A) was chosen as it reflects the actual noise level in thermal power plant of Xinjiang Uyghur Autonomous Region Karamay City. The frequency of noise was 4000 Hz and the sound level for continuous steady noise was 95 dB, both of which were set to be the experimental conditions (Electric audiometer: MIDIMATE 622 Clinical/Diagnostic Audiometer, production date in 2008, Denmark; correction by measurement in the Xinjiang Uygur Autonomous Region Bureau of metrology certification and used within the period of validity). The rats in the experimental group were equally divided into two groups (i.e., five rats in each group) and kept in two cells of the noise chamber (long 1.0 m, wide 1.0 m, high 0.55 m for each cell), where they were exposed to the same amount of noise that was prerecorded using Olympus LS11 recording pen (with an annual output of 2011, Shanghai). The tape player and the loudspeaker were located in the exposure chamber with a distance of 0.4 m from the cells where the rats were kept. Twenty round holes with diameters of 3 cm located on the contact surface between the loudspeaker and the exposure module were used to facilitate the noise transmission. The noise was played with the tape player (Sanyo MCD-XW3292011, Shenzhen, China) and was amplified with the loudspeaker (model: HYS70A-82012, Guangdong, China). We used pressure gauge (HS6288B type noise spectrum analyzer, 2011, Zhejiang, China) to monitor noise intensity during the exposure period. Noise frequency was 4000 Hz, and the average sound intensity was 96 dB(A) (standard deviation [SD] = 1.67). The rats in the control group were kept in the chamber with the same specification as that of the experimental group except for the noise exposure to tease out confounding effects.
Tissue pathology
At the end of the experiment, rats were first anesthetized with an intraperitoneal injection of sodium pentobarbital (50 mg/kg body weight) and then small fragments of brain, heart, liver, and spleen were dissected for electron microscopy. The tissues were labeled, paraffin embedded, serial sectioned immediately after their removal. They were further stained with hematoxylin and eosin.
| Results | | |
Noise exposure comparison
The weighted equivalent continuous perceived noise level values of the experimental group and control group were 105 dB (SD = 1.67) (equivalent continuous A-weighted sound pressure level (LAeq) = 96.1 dB) and 56 dB (SD = 1.21) (LAeq = 48.2 dB), respectively. High-frequency noise exposure in the experimental group was significantly higher than that of the control group (P < 0.01). The criterion for significance was P < 0.05.
Histopathological results
For rats in the control group, the neurons were compactly arranged in the cortex, nucleosomes were clear, and there were few mononuclear cells [Figure 1]. Liver structure was normal, indicating hepatic lobe, liver rope disciple district, and liver ropes were arranged radially around the central vein. No degeneration and necrosis were found in liver cells [Figure 2]. There were no abnormalities showed in the membrane, sheath, germinal center, edge area and junction between red and white pulp in the spleen, and the central artery was round with neither hyperplasia nor atrophy [Figure 3]. There was no swelling observed in myocardial fiber, and both the transverse and longitudinal lines were clear without vessel dilatation and congestion [Figure 4]. Compared with the control group, the most prominent histopathologic changes in brain tissues included loose disorder, hyperemia, edema, expansion of blood vessels, glial cell hyperplasia, and mild atypia in some areas such as hyperchromatic nuclei and irregular karyotype [Figure 5]. There were dilatation and congestion in central vein, hepatic sinus and interlobular veins of liver tissue. The structure of hepatic lobule was destroyed with inflammatory cell infiltrated, and lymphoid nodule was formed [Figure 6]. There was hyperemia in spleen, but the structure was intact. There was extravasated blood, and the splenic sinuses were highly expanded by a blood clot. Hyperplasias of the lymphoid white pulp were also active [Figure 7]. There was dilation and congestion in myocardial interstitial vascular, and there was mild degeneration and hyperemia in myocardial cells. No hemorrhage and myocardial necrosis were observed [Figure 8]. | Figure 1: The control group rat brain tissues (10 × 10) (a). The control group rat brain tissues (10 × 40) (b)
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 | Figure 2: The control group rat liver tissues (10 × 10) (a). The control group rat liver tissues (10 × 40) (b)
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 | Figure 3: The control group rat spleen tissues (10 × 10) (a). The control group rat spleen tissues (10 × 40) (b)
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 | Figure 4: The control group rat heart tissues (10 × 10) (a). The control group rat heart tissues (10 × 40) (b)
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 | Figure 5: The noise-exposed group rat brain tissues (10 × 10) (a). The noise-exposed group rat brain tissues (10 × 40) (b)
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 | Figure 6: The noise-exposed group rat liver tissues (10 × 10) (a). The noise-exposed group rat liver tissues (10 × 40) (b)
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 | Figure 7: The noise-exposed group rat spleen tissues (10 × 10) (a). The noise-exposed group rat spleen tissues (10 × 40) (b)
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 | Figure 8: The noise-exposed group rat heart tissues (10 × 10) (a). The noise-exposed group rat heart tissues (10 × 40) (b)
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| Discussion | | |
The results from this study indicate that high frequency steady noise could lead to various degrees of pathological damages in brain, liver, spleen, and heart tissues of female rats. The pathological changes in rats from the exposed group include loose structure, edema, hyperemia, etc. The possible mechanism leading to this phenomenon is that the brain has three systems, including the dopamine system, amygdala of the limbic system and hippocampal complex system. These systems can be activated by stress factors such as noise. Recent studies have found that [13] the exposure to noise resulted in significant enhancement in the area of collagen-rich connective tissue located in the centrolobular domain of the rat liver. These results were consistent with previous findings, where they showed that fibrotic transformation in rodents and humans was a systemic effect of chronic exposure to industrial wideband noise. Exposure to noise could lead to an increment in dopamine release, and it could also increase the blood viscosity as the materials stored in the platelets of spleen enter to the blood circulation. Moreover, the exposure to noise can induce vascular spasm, resulting in abnormal tissue perfusion, ischemia, and necrosis. Some scholars studied the effects of noise on mice neurons, and they found that cell body density, the nucleolus body density, cell nucleus, and the surface of nucleus of sexually matured rats in the experimental group were significantly different from those in the control group. They further pointed it out that the exposure to noise accelerated the aging process for rats in their premature period. However, the exposure to noise almost had no effect on rats in their old age. It is possible that mice gradually adapted to the environmental noise, and the ear drum has a protective inhibitory effect on the surrounding noise. Recent studies [14],[15],[16] add the liver to a number of other organs (both in humans and rodents) that have been found to enhance their content in collagen fibers after being chronically exposed to noise.
The experiment clearly indicated that the exposure to noise could lead to the pathological changes in liver. One of the possible mechanisms was that the rats could be in a state of stress when they were exposed to noise. Under this circumstance, the oxygen free radicals in the body and malondialdehyde content would be higher than normal, and the malondialdehyde is the product of body's oxygen free radicals and biofilm polyunsaturated fatty acids. This indicated that the exposure to noise increased the level of oxygen free radicals and the lipid peroxidation. Other researchers proposed that noise stimulation in the hearing system may activate degradation of some enzyme in the body or it may inhibit synthetase. These can lead to the damage of protein biosynthesis, which may result in the pathological changes and the malfunction of the liver tissues.
Spleen is an important organ for the immune system, and the pathological changes in spleen are associated with immunosuppression induced by noise. The noise could be considered as a source of stress, which activates the hypothalamic pituitary adrenal axis system. The changes in the body's immune system could results in the neuroendocrine hormone disorders.
Magnesium deficiency could be one of the possible mechanisms associated with the pathological changes in the myocardial structure after the chronic exposure to noise. Some studies showed the cardiac functions of rats that were exposed to high frequency static noise (103 db[A]) 4 h/day for 2 months, have a series problems including disordered arrangement of myocardial cell mitochondria ridge, serious mitochondrial membrane rupture, and myofilament of muscle fiber fracture. Mitochondrial damage, leading to myocardial energy barrier, plus myofilament fracture, will directly affect the cardiac systolic function. Other researchers [17] found that long-term exposure to occupational noise may be associated with an increased risk of ischemic heart disease and all-cause mortality.
| Conclusion | | |
Our experiment demonstrated that the exposure to noise could lead to the pathological changes in brain, liver, spleen, and heart tissues of female rat. However, our study did not fully address the mechanism, and it needs to be further investigated and discussed.
| Acknowledgments | | |
This study is supported by the Karamay Municipal Science and Technology Bureau of Xinjiang, China (No. SK 201146). The Research Ethics Committee of Xinjiang Medical University has provided ethical approval for the conduct of the study on this animal experiment project. Each experiment personnel must undergo medical examination, theoretical training and pass the examination before starting the experiment (Certificate number: 201200026).
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Correspondence Address:
Dr. Laijun Xue
Department of Occupational Diseases, Xinjiang Karamay Municipal Center Hospital, Karamay, Xinjiang 834000
China
 Source of Support: The study is supported by the Karamay Municipal Science and Technology Bureau of Xinjiang, China (No. SK 201146)., Conflict of Interest: None  | Check |
DOI: 10.4103/1463-1741.137048
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8] |
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