Effects of Ascorbic Acid on Oxidative System and Transient Evoked Otoacoustic Emissions in Rabbits Exposed to Noise

Dereköy, Fevzi Sefa; Köken, Tülay; Yılmaz, Deniz; Kahraman, Ahmet; Altuntaş, Ali

doi:10.1097/00005537-200410000-00019

Cited by 26 publications

(17 citation statements)

References 14 publications

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“…As an antioxidant capable of working in both aqueous and nonaqueous environment (22), AA is a good choice of treatment in cases like essential hypertension where an increased free radical production or reduced antioxidant (27,28) level plays an important role in the pathogenesis as well as in long-term complications (29,30). In this study, treatment with ascorbic acid produced a significant reduction in systolic blood pressure in the SHR.…”

Section: Discussionmentioning

confidence: 59%

“…Ascorbic acid (AA), a water soluble antioxidant, provides a strong defense against free radical activity, also has been reported to reduce lipid peroxidation in experimental studies (20,21), and can exert its antioxidant properties in both aqueous and nonaqueous environments (22). Furthermore, AA can potentiate the activity of vitamin E by sparing it, and by further reducing it from the oxidized form (23).…”

Section: Introductionmentioning

confidence: 99%

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Modulation of Nitric Oxide Synthase Activity in Brain, Liver, and Blood Vessels of Spontaneously Hypertensive Rats by Ascorbic Acid: Protection from Free Radical Injury

Newaz

Yousefipour

Nawal

2005

Clinical and Experimental Hypertension

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End organ damage in essential hypertension has been linked to increased oxygen free radical generation, reduced antioxidant defense, and/or attenuation of nitric oxide synthase (NOS) activity. Ascorbic acid (AA), a water-soluble antioxidant, has been reported as a strong defense against free radicals in both aqueous and nonaqueous environment. In this study we examined the hypothesis that antioxidant ascorbic acid may confer protection from increased free radical activity in brain, liver, and blood vessels of spontaneously hypertensive rats (SHR). Male SHRs were divided into groups: SHR + AA (treated with AA, 1 mg/rat/day; for 12 weeks) or SHR (untreated). Wister-Kyoto rats (WKY) served as the control. Mean systolic blood pressure (SBP) in treated and untreated SHR was 145 +/- 7 mmHg and 142 +/- 8 mmHg, respectively. AA treatment prevented the increase in systolic blood pressure in SHR by 37 +/- 1% (p < 0.05). NOS activity in the brain, liver, and blood vessels of WKY rat was 1.82 +/- 0.02, 0.14 +/- 0.003, and 1.54 +/- 0.06 pmol citruline/mg protein, respectively. In SHR, total NOS activity was significantly reduced by 52 +/- 1%, 21 +/- 3%, and 44 +/- 4%, respectively. AA increased NOS activity in brain, liver, and blood vessels of SHR from 0.87 +/-.03, 0.11 +/-.01, and 0.87 +/-.08 pmol citruline/mg protein to 0.93 +/- 0.01, 0.13 +/- 0.001, and 1.11 +/- 0.03 pmol citruline/mg protein (p < 0.05), respectively. Lipid peroxides in the brain, liver, and blood vessels from WKY rats were 0.87 +/- 0.06, 0.11 +/- 0.005, and 0.47 +/- 0.04 nmol MDA equiv/mg protein, respectively. In SHR, lipid peroxides in brain, liver, and blood vessels were significantly increased by 40 +/- 3%, 64 +/- 3%, and 104 +/- 13%, respectively. AA reduced lipid peroxidation in liver and blood vessels by 17 +/- 1% and 34 +/- 3% but not in brain. Plasma lipid peroxides were almost doubled in SHR (p < 0.01) together with a reduction in total antioxidant status (6 +/- 0.1%; p < 0.05), nitrite (53 +/- 2%; p < 0.05) and superoxide dismutase (SOD) activity (36 +/- 2%; p < 0.05). AA treatment reduced plasma lipid peroxide (p < 0.001), and increased TAS (p < 0.001), nitrite (p < 0.001), and SOD activity (p < 0.001). From this study, we conclude that brain, liver, and blood vessels in SHR are susceptible to free radical injury, which reduces the availability of NO either by scavenging it or by reducing its production via inhibiting NOS. In addition, brain, liver, and blood vessels in SHR; may be protected by antioxidant, which improves total antioxidant status, and SOD thus may prevent high blood pressure and its complications.

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Section: Discussionmentioning

confidence: 59%

Section: Introductionmentioning

confidence: 99%

Modulation of Nitric Oxide Synthase Activity in Brain, Liver, and Blood Vessels of Spontaneously Hypertensive Rats by Ascorbic Acid: Protection from Free Radical Injury

Newaz

Yousefipour

Nawal

2005

Clinical and Experimental Hypertension

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“…Other antioxidants that can potentially play a protective role against noise-induced cochlear trauma include ginseng [172], co-enzyme Q10 [177], as well as several vitamins, such as vitamin A [178], vitamin C [179, 180], vitamin E [181, 182], and vitamin B12 [183]. Studies in animals showed a protective benefit from combination antioxidant treatment, such as magnesium and vitamin A, C, and E [184], possibly due to synergistic effects [185–187], These studies were mainly performed in animals or in small groups of humans and the results should be considered preliminary.…”

Section: Pharmacological Treatmentsmentioning

confidence: 99%

Current insights in noise-induced hearing loss: a literature review of the underlying mechanism, pathophysiology, asymmetry, and management options

Le¹,

Straatman²,

Lea³

et al. 2017

J of Otolaryngol - Head & Neck Surg

308

235

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BackgroundNoise-induced hearing loss is one of the most common forms of sensorineural hearing loss, is a major health problem, is largely preventable and is probably more widespread than revealed by conventional pure tone threshold testing. Noise-induced damage to the cochlea is traditionally considered to be associated with symmetrical mild to moderate hearing loss with associated tinnitus; however, there is a significant number of patients with asymmetrical thresholds and, depending on the exposure, severe to profound hearing loss as well.Main bodyRecent epidemiology and animal studies have provided further insight into the pathophysiology, clinical findings, social and economic impacts of noise-induced hearing loss. Furthermore, it is recently shown that acoustic trauma is associated with vestibular dysfunction, with associated dizziness that is not always measurable with current techniques. Deliberation of the prevalence, treatment and prevention of noise-induced hearing loss is important and timely. Currently, prevention and protection are the first lines of defence, although promising protective effects are emerging from multiple different pharmaceutical agents, such as steroids, antioxidants and neurotrophins.ConclusionThis review provides a comprehensive update on the pathophysiology, investigations, prevalence of asymmetry, associated symptoms, and current strategies on the prevention and treatment of noise-induced hearing loss.

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“…That antioxidant agents effectively reduce sensory cell death and NIHL has now been well demonstrated in animal studies using a variety of antioxidant agents, such as GSH/ glutathione monoethyl ester (GSHE) (Ohinata et al, 2000b;Kopke et al, 2002;Hight et al, 2003;Miller et al, 2003a), resveratrol (Seidman et al, 2003), allopurinol (Seidman et al, 1993;Cassandro et al, 2003), superoxide dismutase-polyethylene glycol (Seidman et al, 1993), U74389F (a lazaroid drug which inhibits lipid peroxidation and scavenges free radicals) (Quirk et al, 1994), and R-phenylisopropyladenosine (R-PIA) (Hu et al, 1997;Hight et al, 2003). Small protective effects of individual (or combined) dietary antioxidant nutrients are also well described for insults to the inner ear including noise, drugs, and age (Chole and Quick, 1976;Lohle, 1980Lohle, ,1985Romeo, 1985;Biesalski et al, 1990;Lopez-Gonzalez et al, 2000;Seidman, 2000;Bertolaso et al, 2001;Pasqualetti and Rijli, 2001;Teranishi et al, 2001;Rabinowitz et al, 2002;Hou et al, 2003;Derekoy et al, 2004;Kalkanis et al, 2004;Weijl et al, 2004;Ahn et al, 2005;McFadden et al, 2005;Yamashita et al, 2005a).…”

Section: Enhancing Antioxidant Defense Attenuates Nihlmentioning

confidence: 99%

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

et al. 2007

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Recent research has shown the essential role of reduced blood flow and free radical formation in the cochlea in noise-induced hearing loss (NIHL). The amount, distribution, and time course of free radical formation have been defined, including a clinically significant late formation 7-10 days following noise exposure, and one mechanism underlying noise-induced reduction in cochlear blood flow has finally been identified. These new insights have led to the formulation of new hypotheses regarding the molecular mechanisms of NIHL; and, from these, we have identified interventions that prevent NIHL, even with treatment onset delayed up to 3 days post-noise. It is essential to now assess the additive effects of agents intervening at different points in the cell death pathway to optimize treatment efficacy. Finding safe and effective interventions that attenuate NIHL will provide a compelling scientific rationale to justify human trials to eliminate this single major cause of acquired hearing loss.

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Effects of Ascorbic Acid on Oxidative System and Transient Evoked Otoacoustic Emissions in Rabbits Exposed to Noise

Cited by 26 publications

References 14 publications

Modulation of Nitric Oxide Synthase Activity in Brain, Liver, and Blood Vessels of Spontaneously Hypertensive Rats by Ascorbic Acid: Protection from Free Radical Injury

Modulation of Nitric Oxide Synthase Activity in Brain, Liver, and Blood Vessels of Spontaneously Hypertensive Rats by Ascorbic Acid: Protection from Free Radical Injury

Current insights in noise-induced hearing loss: a literature review of the underlying mechanism, pathophysiology, asymmetry, and management options

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

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