Noise-induced changes in expression levels of NADPH oxidases in the cochlea

Vlajkovic, Srdjan M.; Lin, Shelly C. Y.; Wong, Ann Chi Yan; Wackrow, Brad; Thorne, Peter R.

doi:10.1016/j.heares.2013.07.012

Cited by 51 publications

(49 citation statements)

References 29 publications

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“…In addition, lead-induced oxidative stress in the cochlea was also indicated by the increase in the expression of Sod3, which encodes for extracellular superoxide dismutase, and Gstp1, which encodes for cytosolic glutathione transferase. Although the levels of Nox4 and Fmo2 were decreased after lead exposure, these changes may not reflect the overall cochlear oxidative stress because Nox4 is just one of the many NADPH oxidase isoforms expressed in the cochlea (Banfi et al, 2004; Vlajkovic et al, 2013) and reactive oxygen species could be generated by other pro-oxidant genes that are more abundantly expressed in the cochlea.…”

Section: Discussionmentioning

confidence: 99%

Chronic lead exposure induces cochlear oxidative stress and potentiates noise-induced hearing loss

et al. 2018

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Acquired hearing loss is caused by complex interactions of multiple environmental risk factors, such as elevated levels of lead and noise, which are prevalent in urban communities. This study delineates the mechanism underlying lead-induced auditory dysfunction and its potential interaction with noise exposure. Young-adult C57BL/6 mice were exposed to: 1) control conditions; 2) 2 mM lead acetate in drinking water for 28 days; 3) 90 dB broadband noise 2 h/day for two weeks; and 4) both lead and noise. Blood lead levels were measured by inductively coupled plasma mass spectrometry analysis (ICP-MS) lead-induced cochlear oxidative stress signaling was assessed using targeted gene arrays, and the hearing thresholds were assessed by recording auditory brainstem responses. Chronic lead exposure downregulated cochlear Sod1, Gpx1, and Gstk1, which encode critical antioxidant enzymes, and upregulated ApoE, Hspa1a, Ercc2, Prnp, Ccl5, and Sqstm1, which are indicative of cellular apoptosis. Isolated exposure to lead or noise induced 8–12 dB and 11–25 dB shifts in hearing thresholds, respectively. Combined exposure induced 18–30 dB shifts, which was significantly higher than that observed with isolated exposures. This study suggests that chronic exposure to lead induces cochlear oxidative stress and potentiates noise-induced hearing impairment, possibly through parallel pathways.

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Section: Discussionmentioning

confidence: 99%

Chronic lead exposure induces cochlear oxidative stress and potentiates noise-induced hearing loss

et al. 2018

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“…Overall, the noise levels varied less than ± 1 dB (100 ± 1 dB) (18) between the measuring points and the frequency distribution of the noise matched with high-pass white noise spectrum. Such spectrum (HPWN/8kHz) was selected to cause hearing losses where auditory sensitivity is the highest for the rats (19). The cages in the chambers were daily rotated to maintain the most equal exposure for all rats.…”

Section: Methodsmentioning

confidence: 99%

Oxidative stress indices in rats’ lung tissues following simultaneous exposure to noise and styrene

Haghighat

Khavanin

Allameh

2017

JOHE

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Received: April 2017, Accepted: May 2017 Background: Simultaneous exposure to noise and organic solvents such as styrene is an indispensable part of today's industries. Numerous studies were done related to ototoxic effects of coexposure to noise and styrene while some evidences showed the adverse effects of such exposure on other organs. In this study, we aimed to assess the subacute effects of combined exposure to noise and styrene on rats' lung tissue. Materials and Methods: Twenty-four Wistar male rats were divided in four groups including: A) control, B) rats exposed to 100 dB octave band of noise, C) rats exposed to 750 ppm styrene alone, and D) rats exposed to combination of 100 dB noise and 750 ppm styrene. Following the last day of exposure, the rats were euthanized and their lung tissues were excised, homogenized and assayed for biological analysis of malondialdehyde (MDA), glutathione (GSH), catalase (CAT) and superoxide dismutase (SOD). The results were analyzed using SPSS software. Results: MDA increased significantly (P < 0.001) at the end of experiment in the group exposed to styrene and noise-styrene. GSH concentrations decreased significantly in styrene and noise-styrene group (P < 0.001). SOD (P < 0.001) and CAT (P < 0.05) activities were determined to be significantly lower for the styrene and noise-styrene groups compared to the control group. Conclusions: In conclusion, our results indicated that exposure to combination of noise and styrene caused oxidative stress, increased lipid peroxidation, and antioxidant depletion. These results appear to support the fact that co-exposure to noise and styrene might cause oxidative stress-induced damage to the lung tissue. Since simultaneous exposure to noise and styrene has an additive effect in this regard, further studies are necessary to be carried out on the effects of noise and organic solvents coexposure.

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“…In support of this contention, NOX3 knockout mice have been reported to show signs of imbalance [102]. In addition, reduction of NOX3 has been implicated to have a protective effect in cochlear injury by reducing the amount of oxidative stress produced [103]. NOX3 generates superoxide as its product, and the regulatory mechanism of NOX3 can involve Rac1, NOXO1, and p67phox [40, 64, 104].…”

Section: Introductionmentioning

confidence: 99%

“…DUOX1 has been reported to mediate allergic asthma [121], prolong ROS generation after irradiation [122], and play a role in cancer development [123]. DUOX2 has been reported to mediate keratinocyte inflammation [124], cochlear injury [103], and lung injury [125]. Furthermore, both DUOX enzymes have been implicated to be important in ROS-dependent immunity [126].…”

Section: Introductionmentioning

confidence: 99%

NADPH oxidase in brain injury and neurodegenerative disorders

Merry

Wang

Zhang

et al. 2017

Mol Neurodegeneration

342

309

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Oxidative stress is a common denominator in the pathology of neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and multiple sclerosis, as well as in ischemic and traumatic brain injury. The brain is highly vulnerable to oxidative damage due to its high metabolic demand. However, therapies attempting to scavenge free radicals have shown little success. By shifting the focus to inhibit the generation of damaging free radicals, recent studies have identified NADPH oxidase as a major contributor to disease pathology. NADPH oxidase has the primary function to generate free radicals. In particular, there is growing evidence that the isoforms NOX1, NOX2, and NOX4 can be upregulated by a variety of neurodegenerative factors. The majority of recent studies have shown that genetic and pharmacological inhibition of NADPH oxidase enzymes are neuroprotective and able to reduce detrimental aspects of pathology following ischemic and traumatic brain injury, as well as in chronic neurodegenerative disorders. This review aims to summarize evidence supporting the role of NADPH oxidase in the pathology of these neurological disorders, explores pharmacological strategies of targeting this major oxidative stress pathway, and outlines obstacles that need to be overcome for successful translation of these therapies to the clinic.

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Noise-induced changes in expression levels of NADPH oxidases in the cochlea

Cited by 51 publications

References 29 publications

Chronic lead exposure induces cochlear oxidative stress and potentiates noise-induced hearing loss

Chronic lead exposure induces cochlear oxidative stress and potentiates noise-induced hearing loss

Oxidative stress indices in rats’ lung tissues following simultaneous exposure to noise and styrene

NADPH oxidase in brain injury and neurodegenerative disorders

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