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45 results for “Ototoxicity”
Pterostilbene Protects Cochlea from Ototoxicity in Streptozotocin-Induced Diabetic Rats by Inhibiting Apoptosis
<p>Diabetes mellitus (DM) causes ototoxicity by inducing oxidative stress, microangiopathy, and apoptosis in the cochlear sensory hair cells. The natural anti-oxidant pterostilbene (PTS) (trans-3,5-dimethoxy-4-hydroxystylbene) has been reported to relieve oxidative stress and apoptosis in DM, but its role in diabetic-induced ototoxicity is unclear. This study aimed to investigate the effects of dose-dependent PTS on the cochlear cells of streptozotocin (STZ)-induced diabetic rats. The study included 30 albino male Wistar rats that were randomized into five groups: non-diabetic control (Control), diabetic control (DM), and diabetic rats treated with intraperitoneal PTS at 10, 20, or 40 mg/kg/day during the four-week experimental period (DM + PTS10, DM + PTS20, and DM + PTS40). Distortion product otoacoustic emission (DPOAE) tests were performed at the beginning and end of the study. At the end of the experimental period, apoptosis in the rat cochlea was investigated using caspase-8, cytochrome-c, and terminal deoxyribonucleotidyl transferase-mediated dUTP-biotin end labeling (TUNEL). Quantitative real-time polymerase chain reaction was used to assess the mRNA expression levels of the following genes: CASP-3, BCL-associated X protein (BAX), and BCL-2. Body weight, blood glucose, serum insulin, and malondialdehyde (MDA) levels in the rat groups were evaluated. The mean DPOAE amplitude in the DM group was significantly lower than the means of the other groups (0.9–8 kHz; P < 0.001 for all). A dose-dependent increase of the mean DPOAE amplitudes was observed with PTS treatment (P < 0.05 for all). The Caspase-8 and Cytochrome-c protein expressions and the number of TUNEL-positive cells in the hair cells of the Corti organs of the DM rat group were significantly higher than those of the PTS treatment and control groups (DM > DM + PTS10 > DM + PTS20 > DM + PTS40 > Control; P < 0.05 for all). PTS treatment also reduced cell apoptosis in a dose-dependent manner by increasing the mRNA expression of the anti-apoptosis BCL2 gene and by decreasing the mRNA expressions of both the pro-apoptosis BAX gene and its effector CASP-3 and the ratio of BAX/BCL-2 in a dose-dependent manner (P < 0.05 compared to DM for all). PTS treatment significantly improved the metabolic parameters of the diabetic rats, such as body weight, blood glucose, serum insulin, and MDA levels, consistent with our other findings (P < 0.05 compared to DM for all). PTS decreased the cochlear damage caused by diabetes, as confirmed by DPOAE, biochemical, histopathological, immunohistochemical, and molecular findings. This study reports the first in vivo findings to suggest that PTS may be a protective therapeutic agent against diabetes-induced ototoxicity.</p>
Protective role of Pyrroloquinoline quinone against gentamicin induced cochlear hair cell ototoxicity
<p><strong>Abstract:</strong> Gentamicin(GM) is one of the commonly used antibiotics in the aminoglycoside class but ototoxicity as a side effect constantly impacts the quality of human life. Pyrroloquinoline quinone (PQQ) as a redox cofactor produced by bacteria was found in soil and foods that exert an antioxidant and redox modulator. It is well documented that the PQQ can alleviate inflammatory responses and cytotoxicity. However, our understanding of PQQ in ototoxicity remains unclear. We reported that PQQ could protect against GM-induced ototoxicity in House Ear Institute-Organ of Corti 1 (HEI-OC1) cells<em> in vitro</em>. To evaluate reactive oxygen species production and mitochondrial function, ROS and JC-1 staining, oxygen consumption rate (OCR), and extracellular acidification rate (ECAR) measurements in living cells, mitochondrial dynamics analysis was performed. GM-mediated damage by reducing the production of ROS and inhibiting mitochondria biogenesis and dynamics. PQQ ameliorated the cellular oxidative stress, and recovered mitochondrial membrane potential, facilitating the recovery of mitochondrial biogenesis and dynamics. Our <em>in vitro</em> findings improve our understanding of GM-induced ototoxicity with therapeutic implications for PQQ.</p>
Randomized Trial Comparison of Ototoxicity Monitoring Programs
ClinicalTrials.gov study NCT02099786. IPD Sharing: NO. Countries: 1. Publications: 8.
SPI-1005 for Prevention and Treatment of Tobramycin Induced Ototoxicity
ClinicalTrials.gov study NCT02819856. IPD Sharing: UNDECIDED. Countries: 1. Publications: 5.
Preventing Nephrotoxicity and Ototoxicity From Osteosarcoma Therapy
ClinicalTrials.gov study NCT01848457. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Protective Effect of N-acetylcysteine Against From Ototoxicity
ClinicalTrials.gov study NCT01271088. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Prevention of Ototoxicity in NTM Patients Treated With IV Amikacin
ClinicalTrials.gov study NCT05730283. IPD Sharing: NO. Countries: 1. Publications: 12.
The Protective Effect of Ginkgo Biloba Extract on Cisplatin-induced Ototoxicity in Humans
ClinicalTrials.gov study NCT01139281. IPD Sharing: Not stated. Countries: 1. Publications: 56.
Video Game Hearing Tests for Remote Monitoring of Ototoxicity
ClinicalTrials.gov study NCT05847556. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Transtympanic Ringer's Lactate for the Prevention of Cisplatin Ototoxicity
ClinicalTrials.gov study NCT01108601. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Prevention of Drug Induced Ototoxicity in Peritoneal Dialysis Patients by N-Acetylcysteine
ClinicalTrials.gov study NCT01131468. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Evaluation of the Effect of Rosuvastatin on Cisplatin-induced Nephrotoxicity and Ototoxicity
ClinicalTrials.gov study NCT04817904. IPD Sharing: NO. Countries: 1. Publications: 4.
Protective Effect of Acetylcysteine Against Cisplatinum-Induced Ototoxicity: A Randomized Controlled Trial
ClinicalTrials.gov study NCT07364747. IPD Sharing: NO. Countries: 1. Publications: 0.
SENS-401 to Prevent the Ototoxicity Induced by Cisplatin in Adult Subjects With a Neoplastic Disease
ClinicalTrials.gov study NCT05628233. IPD Sharing: NO. Countries: 1. Publications: 0.
Sodium Thiosulfate in Preventing Ototoxicity for Squamous Cell Cancer Patients Undergoing Chemoradiation With Cisplatin
ClinicalTrials.gov study NCT04541355. IPD Sharing: NO. Countries: 1. Publications: 0.
Impact on Quality of Life of Long-term Ototoxicity in Cancer Survivors
ClinicalTrials.gov study NCT04281953. IPD Sharing: NO. Countries: 1. Publications: 0.
Effect of subchronic ototoxic (streptomycin) exposure on the vestibular epithelium of the rat
GEO Series GSE292473. Rattus norvegicus. 6 samples. Type: Expression profiling by high throughput sequencing.
Effect of subchronic (4 weeks) ototoxic (3,3'-iminodipropionitrile - IDPN) exposure on the vestibular epithelium of the rat
GEO Series GSE292470. Rattus norvegicus. 6 samples. Type: Expression profiling by high throughput sequencing.
Effect of subchronic ototoxic (3,3'-iminodipropionitrile - IDPN) exposure on the vestibular epithelium of the mouse
GEO Series GSE292468. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
Leveraging large-scale datasets and single cell omics data to develop a polygenic score for cisplatin-induced ototoxicity
GEO Series GSE281324. Mus musculus. 4 samples. Type: Expression profiling by high throughput sequencing.
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