ototoxicity/arginine

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Amelioration of Cisplatin-Induced Ototoxicity in Rats by L-arginine: The Role of Nitric Oxide, Transforming Growth Factor Beta 1 and Nrf2/HO-1 Pathway

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rong class="sub-title"> Background: rong> Cisplatin is an alkylating agent that inhibits DNA replication and interferes with proliferation of cancer cells. However, the major limiting factor for its use is the possible development of adverse effects, including

Nitro-L-arginine methyl ester: a potential protector against gentamicin ototoxicity.

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The nitric oxide (NO) inhibitor nitro-L-arginine methyl ester (L-NAME) may act as an otoprotectant against high-frequency hearing loss caused by gentamicin, but further studies are needed to confirm this.Aminoglycoside antibiotics are still widely used by virtue of their efficacy and low cost. Their

Cisplatin-induced ototoxicity involves interaction of PRMT3 and cannabinoid system.

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This study investigated whether protein arginine methyltransferase (PRMT) and the cannabinoid system are involved in cisplatin-induced ototoxicity. Cisplatin increased cytosine-cytosine-adenosine-adenosine-thymidine-enhancer-binding protein homologous protein expression. This effect is indicative of

Protective effect of brain-derived neurotrophic factor against the ototoxicity of Pseudomonas aeruginosa exotoxin A.

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OBJECTIVE The protective effect of brain-derived neurotrophic factor (BDNF) against the ototoxicity resulting from exposure of Pseudomonas aeruginosa exotoxin A (PaExoA) to the middle ear was analyzed. The combined effect of BDNF and N(G)-nitro-L-arginine methyl ester (L-NAME) was also

Protective Efect of Brain-derived Neurotrophic Factor Against the Ototoxicity of Pseudomonas aeruginosa Exotoxin A.

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Objective--The protective effect of brain-derived neurotrophic factor (BDNF) against the ototoxicity resulting from exposure of Pseudomonas aeruginosa exotoxin A (PaExoA) to the middle ear was analyzed. The combined effect of BDNF and NG-nitro-L-arginine methyl ester (L-NAME) was also investigated.

N-acetylcysteine and N-nitroarginine methyl ester attenuate Carboplatin-induced ototoxicity in dissociated spiral ganglion neuron cultures.

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OBJECTIVE Carboplatin, a platinum-containing anti-cancer drug used to treat a variety of cancers, induces ototoxicity. Since, reactive oxygen species (ROS) and nitric oxide (NO) seem to be responsible for this toxicity, the antioxidant, N-acetyl-L-cysteine (L-NAC), and NO synthetase inhibitor,

Inhibition of Protein arginine methyltransferase 6 reduces reactive oxygen species production and attenuates aminoglycoside- and cisplatin-induced hair cell death.

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Hair cells in the inner ear have been shown to be susceptible to ototoxicity from some beneficial pharmaceutical drugs, such as aminoglycosides and cisplatin. Thus, there is great interest in discovering new targets or compounds that protect hair cells from these ototoxic drugs. Epigenetic

Ototoxicity of sodium nitroprusside.

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Nitric oxide (NO) not only has normal physiological roles like vasodilation and neurotransmission in the living organism, it could also have possible neurodestructive effects under certain pathological conditions. The present study aimed to determine whether direct exposure of guinea pig cochlea to

Brain-derived neurotrophic factor and nitric oxide synthase inhibitor protect the vestibular organ against gentamicin ototoxicity.

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In order to find a way to develop a new treatment for inner ear disorders, the effects of a nitric oxide synthase (NOS) inhibitor [N-nitro-L-arginine methylester (L-NAME)] and a neurotrophin [brain-derived neurotrophic factor (BDNF)] were investigated. The effect of L-NAME and BDNF on

The production of free oxygen radicals and nitric oxide in the rat cochlea.

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Rat cochleas were analysed for free oxygen radicals (FOR) and nitric oxide (NO) production by the chemiluminescent oxidation of luminol. 4Beta-phorbol-12beta-myristate-13alpha-acetate (PMA), a well-known agonist of protein kinase C, induced the release of FOR after a time lag close to 30 s and

Nitric oxide synthase inhibitor reduces the apoptotic change in the cisplatin-treated cochlea of guinea pigs.

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Cisplatin is known to cause inner ear damage. The role of nitric oxide (NO) in the cochlea of the guinea pigs after injections of cisplatin or a combination of cisplatin and NO synthase (NOS) inhibitor [N(G)-nitro-L-arginine methyl ester (L-NAME)] i.p. was examined by means of immunohistochemistry.

Pharmacological models for inner ear therapy with emphasis on nitric oxide.

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Nitric oxide (NO)-mediated neurotoxicity may be an appropriate pathophysiological model with which to explain a variety of inner ear diseases characterized by acute or progressive hearing loss, tinnitus and vertigo. The localization of NO synthase (NOS) isoforms was examined in the inner ear of the

Nitric oxide synthase inhibitor suppresses the ototoxic side effect of cisplatin in guinea pigs.

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Cisplatin is known to cause inner ear damage (ototoxicity). The role of inducible nitric oxide synthase (iNOS) in the cochlea of guinea pigs after injections of cisplatin or a combination of cisplatin and NOS inhibitor (NG-nitro-L-arginine methyl ester, L-NAME) i.p. was examined electro-and

Free radicals in the guinea pig inner ear following gentamicin exposure.

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The purpose of this study was to investigate the occurrence of free radicals, nitric oxide (NO), superoxide (O-2) and peroxynitrite, in the inner ear of the guinea pig following intratympanic injection with 5 mg of gentamicin (GM). Forty-eight hours after GM injection, varying degrees of

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