Oxidative DNA damage is associated with intense noise exposure in the rat

Campen, Luann E. Van; Murphy, William J.; Franks, John R.; Mathias, Patricia I.; Toraason, Mark

doi:10.1016/s0378-5955(01)00391-4

Cited by 115 publications

(59 citation statements)

References 41 publications

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“…They cause breakdown of lipid molecules of cell membrane which is known as lipid peroxidation as well as impairment of proteins and deoxyribonucleic acid (DNA) (Van Campen et al 2002). Under normal conditions, the endogenous antioxidants protect the cell from the damaging effect of free oxygen radicals (Henderson et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Effect of noise stress on cardiovascular system in adult male albino rat: implication of stress hormones, endothelial dysfunction and oxidative stress

Said¹,

El-Gohary²

2016

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Abstract. Noise pollution has been realized as an environmental stressor associated with modern life style that affects our health without being consciously aware of it. The present study investigated the effect of acute, chronic intermittent and chronic continuous exposure to noise of intensity 80-100 dB on heart rate and mean systemic arterial blood pressure in rats and the possible underlying mechanisms. Noise stress causes significant increase in heart rate, mean systemic arterial blood pressure as well as significant increase in plasma levels of corticosterone, adrenaline, noradrenaline, endothelin-1, nitric oxide and malondialdehyde with significant decrease in superoxide dismutase and these values are significantly more worse in chronic continuous exposure to noise than acute or chronic intermittent exposure. These findings suggest that noise stress has many adverse effects on cardiovascular system via increasing plasma levels of stress hormones, oxidative stress and endothelial dysfunction. These findings have major implication in the management of adverse cardiovascular reactions of people subjected to daily noise stress.

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Section: Discussionmentioning

confidence: 99%

Effect of noise stress on cardiovascular system in adult male albino rat: implication of stress hormones, endothelial dysfunction and oxidative stress

Said¹,

El-Gohary²

2016

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“…cisplatin (2,3), aminoglycoside antibiotics (3)) or to noise (4). Signs of oxidative stress, such as DNA damage and lipid peroxidation, have been documented in vivo in response to those challenges (5,6), as well as in cochlear aging (7). The vestibular system is also damaged by ototoxic drugs (8,9) in a process that includes excessive ROS production (10,11).…”

mentioning

confidence: 99%

NOX3, a Superoxide-generating NADPH Oxidase of the Inner Ear

Bánfi

Malgrange

Knisz³

et al. 2004

Journal of Biological Chemistry

401

349

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Reactive oxygen species (ROS) play a major role in drug-, noise-, and age-dependent hearing loss, but the source of ROS in the inner ear remains largely unknown. Herein, we demonstrate that NADPH oxidase (NOX) 3, a member of the NOX/dual domain oxidase family of NADPH oxidases, is highly expressed in specific portions of the inner ear. As assessed by real-time PCR, NOX3 mRNA expression in the inner ear is at least 50-fold higher than in any other tissues where its expression has been observed (e.g. fetal kidney, brain, skull). Microdissection and in situ hybridization studies demonstrated that NOX3 is localized to the vestibular and cochlear sensory epithelia and to the spiral ganglions. Transfection of human embryonic kidney 293 cells with NOX3 revealed that it generates low levels of ROS on its own but produces high levels of ROS upon co-expression with cytoplasmic NOX subunits. NOX3-dependent superoxide production required a stimulus in the absence of subunits and upon co-expression with phagocyte NADPH oxidase subunits p47 phox and p67 phox , but it was stimulus-independent upon co-expression with colon NADPH oxidase subunits NOX organizer 1 and NOX activator 1. Pre-incubation of NOX3-transfected human embryonic kidney 293 cells with the ototoxic drug cisplatin markedly enhanced superoxide production, in both the presence and the absence of subunits. Our data suggest that NOX3 is a relevant source of ROS generation in the cochlear and vestibular systems and that NOX3-dependent ROS generation might contribute to hearing loss and balance problems in response to ototoxic drugs.The inner ear is a highly complex structure involved in hearing and balancing. The conversion of sound into electrical signals occurs within the cochlea, in the organ of Corti, and the electrical signals are conducted by the axons of spiral ganglion neurons to the brain. The linear movement of the head is sensed by the otolith organs (utricle and saccule) and the rotation movements by the ampulla of the semicircular canals. The signals generated in the vestibular system are transmitted by the vestibular ganglion neurons to the central nervous system.Hearing impairment caused by loss of cochlear function occurs frequently, if not invariably, over a lifetime. Noise and ototoxic chemicals may lead to a precocious, rapid hearing loss, whereas aging leads to a more insidious, chronic loss of hearing. Research over the last decades has identified reactive oxygen species (ROS) 1 as the major factor mediating hearing loss (1). ROS is generated within the cochlea after exposure to ototoxic drugs (e.g. cisplatin (2, 3), aminoglycoside antibiotics (3)) or to noise (4). Signs of oxidative stress, such as DNA damage and lipid peroxidation, have been documented in vivo in response to those challenges (5, 6), as well as in cochlear aging (7). The vestibular system is also damaged by ototoxic drugs (8, 9) in a process that includes excessive ROS production (10, 11).Although the role of oxidative stress in inner ear damage is well established, its source ...

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“…Damage in the brain and liver was detected 3 days after the exposure. [11] In yet another study, Manikandan et al found increased MDA levels in different areas of the brain after 30 days of 100 dB white noise exposure, and Srikumar and colleagues in their study found increased levels of MDA in the serum, thymus gland, and spleen tissue after a 15-day exposure to white noise. [10,13] Similarly, high levels of lipid peroxidation have been indicated in other studies as an indirect sign of increased ROS production in the serum and different areas of the brain during acute, subacute, and chronic noise exposure.…”

Section: Discussionmentioning

confidence: 95%

“…[7][8][9] There are many studies in the literature showing that the auditory, the auditory pathways, and brain can be damaged by exposure to environmental noise. [10][11][12][13] However, the effects of statins on cerebral oxidative damage induced by noise have not been investigated to date. Therefore, we decided to determine in this study whether noise results in oxidative stress in rat brain tissue, as well as examine the possible effect of rosuvastatin.…”

Section: Introductionmentioning

confidence: 99%

Possible effects of rosuvastatin on noise-induced oxidative stress in rat brain

et al. 2014

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The problem of noise has recently gained more attention as it has become an integral part of our daily lives. However, its influence has yet to be fully elucidated. Other than being an unpleasant stimulus, noise may cause health disorders through annoyance and stress, including oxidative stress. Rosuvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, may possess antioxidant properties. Based on rat models, our project investigates the effect of rosuvastatin on noise-induced oxidative stress in the brain tissue. Thirty-two male Wistar albino rats were used. The rats were divided into four groups: Noise exposure plus rosuvastatin usage, only noise exposure, only rosuvastatin usage, and control. After the data had been collected, oxidant and antioxidant parameters were analyzed in the cerebral cortex, brain stem, and cerebellum. Results indicated that superoxide dismutase values were significantly decreased in the cerebral cortex, while malondialdehyde values in the brainstem and cerebellum were significantly increased in the group with only noise exposure. Superoxide dismutase values in the brainstem were significantly increased, but nitric oxide values in the cerebellum and brainstem and malondialdehyde values in the cerebellum and cerebral cortex were significantly decreased in the group where only rosuvastatin was used. During noise exposure, the use of rosuvastatin caused significantly increased superoxide dismutase values in the cerebral cortex and brainstem, but significantly reduced malondialdehyde values in the brain stem. Consequently, our data show that brain tissue was affected by oxidative stress due to continued exposure to noise. This noise-induced stress decreases with rosuvastatin therapy.

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Oxidative DNA damage is associated with intense noise exposure in the rat

Cited by 115 publications

References 41 publications

Effect of noise stress on cardiovascular system in adult male albino rat: implication of stress hormones, endothelial dysfunction and oxidative stress

Effect of noise stress on cardiovascular system in adult male albino rat: implication of stress hormones, endothelial dysfunction and oxidative stress

NOX3, a Superoxide-generating NADPH Oxidase of the Inner Ear

Possible effects of rosuvastatin on noise-induced oxidative stress in rat brain

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