8-hydroxy-2--deoxyguanosine and Hearing-Loss--Noise-Induced

This study aimed to explore the molecular mechanism of the protective effects of hydrogen-saturated saline on NIHL.. Guinea pigs were divided into three groups: hydrogen-saturated saline; normal saline; and control. For saline administration, the guinea pigs were given daily abdominal injections 3 d before and 1 h before noise exposure. ABR were tested to examine cochlear physiology changes. The changes of 8-hydroxy-desoxyguanosine (8-HOdG), interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor-α (TNF-α), intercellular cell adhesion molecule-1 (ICAM-1) and high mobility group box-1 protein (HMGB1) in the cochlea were also examined.. The results showed that pre-treatment with hydrogen-saturated saline could significantly attenuate noise-induced hearing loss. The concentration of 8-HOdG was also significantly decreased in the hydrogen-saturated saline group compared with the normal saline group. After noise exposure, the concentrations of IL-1, IL-6, TNF-α, and ICAM-1 in the cochlea of guinea pigs in the hydrogen-saturated saline group were dramatically reduced compared to those in the normal saline group. The concentrations of HMGB-1 and IL-10 in the hydrogen-saturated saline group were significantly higher than in those in the normal saline group immediately and at 7 d after noise exposure.. This study revealed for the first time the protective effects of hydrogen-saturated saline on noise-induced hearing loss (NIHL) are related to both the anti-oxidative activity and anti-inflammatory activity.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Animals; Cochlea; Cytokines; Deoxyguanosine; Disease Models, Animal; Evoked Potentials, Auditory, Brain Stem; Female; Guinea Pigs; Hearing Loss, Noise-Induced; Hydrogen; Inflammation Mediators; Male; Sodium Chloride

Evaluating the correlation between otoacoustic emission levels, styrene exposure, and oxidative stress biomarkers concentration in styrene-exposed subjects, to investigate the role of oxidative stress in outer hair cell damage.. Distortion product otoacoustic emissions were measured in the exposed workers and in a control group. Separation between the distortion and reflection otoacoustic components was performed by time-frequency-domain filtering. The urinary concentration of the DNA and RNA oxidation products, namely 8-oxo-7,8-dihydroguanine (oxoGua), 8-oxo-7,8-dihydro-2'-deoxyguanosine (oxodGuo), and 8-oxo-7,8-dihydroguanosine (oxoGuo), were evaluated.. Nine subjects exposed to styrene in a fiberglass factory, eight control subjects. The two groups were statistically equivalent in mean age.. Statistically significant differences were found in the distortion component levels between the exposed and the control group. High levels of the oxidative damage biomarkers were found in the workers exposed to high levels of styrene. Significant negative correlation was found between the otoacoustic emission distortion component levels and the concentration of the oxoGuo biomarker.. Exposure-induced damage of the cochlear amplifier is shown in the mid-frequency range, confirming animal experiments, in which hair cells in the cochlear middle turn were damaged. Hearing damage is consistent with the outer hair cell apoptosis pathway associated with oxidative stress.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Acoustics; Adult; Apoptosis; Biomarkers; Case-Control Studies; Deoxyguanosine; DNA Damage; Female; Guanine; Guanosine; Hair Cells, Auditory, Outer; Hearing Loss, Noise-Induced; Hearing Tests; Humans; Male; Middle Aged; Noise, Occupational; Occupational Diseases; Occupational Exposure; Occupational Health; Otoacoustic Emissions, Spontaneous; Oxidative Stress; Risk Factors; Styrene

Reactive oxygen species (ROS) that form in the inner ear play an important role in noise-induced hearing loss (NIHL). Recent studies have revealed that molecular hydrogen (H2) has great potential for reducing ROS. In this study, we examined the potential of hydrogen gas to protect against NIHL. We tested this hypothesis in guinea pigs with 0.5%, 1.0% and 1.5% H2 inhalation in air for 5h a day after noise exposure, for five consecutive days. All animals underwent measurements for auditory brainstem response after the noise exposure; the results revealed that there was a better improvement in the threshold shift for the 1.0% and 1.5% H2-treated groups than the non-treated group. Furthermore, outer hair cell (OHC) loss was examined 7 days after noise exposure. A significantly higher survival rate of OHCs was observed in the 1.0% and 1.5% H2-treated group as compared to that of the non-treated group in the basal turn. Immunohistochemical analyses for 8-hydroxy-2'-deoxyguanosine (8-OHdG) were performed to examine the amount of oxidative DNA damage. While strong immunoreactivities against 8-OHdG were observed of the non-treated group, the H2-treated group showed decreased immunoreactivity for 8-OHdG. These findings strongly suggest that inhaled hydrogen gas protects against NIHL.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Administration, Inhalation; Animals; Cell Count; Cell Survival; Deoxyguanosine; Evoked Potentials, Auditory, Brain Stem; Female; Guinea Pigs; Hair Cells, Auditory, Outer; Hearing Loss, Noise-Induced; Hydrogen; Neuroprotective Agents; Reactive Oxygen Species

Increasing evidence suggests that noise-induced hearing loss may be reduced or prevented with antioxidant therapy. Biochemical markers of reactive oxygen species (ROS)-induced damage can help elucidate possible treatment timing constraints. This study examined the time course of ROS damage following a 2-h, broad-band noise exposure resulting in permanent threshold shift in 35 Long-Evans rats. Cochlea, brain, liver, serum and urine were analyzed at 1, 3, 8, 72, and 672 h (28 days) after exposure. Oxidative DNA damage was assessed by measuring 8-hydroxy-2'-deoxyguanosine (8OHdG) by high performance liquid chromatography with electrochemical detection. Lipid peroxidation was measured via the thiobarbituric acid-reactive substances (TBARS) colorimetric assay for detection of aldehydes (e.g., malondialdehyde). Auditory brainstem response and distortion product otoacoustic emission thresholds showed progressive elevation for the 3- and 8-h groups, then notable recovery for the 72-h group, and some worsening for the 672-h group. 8OHdG was significantly elevated in cochlea in the 8-h group, and in brain and liver for the 72-h group. TBARS were significantly elevated in serum for the 72-h group. Based upon oxidative DNA damage present in cochlea following intense noise, we postulate that the first 8 h following exposure might be a critical period for antioxidant treatment.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Animals; Antioxidants; Brain; Cochlea; Deoxyguanosine; DNA Damage; Evoked Potentials, Auditory, Brain Stem; Hearing Loss, Noise-Induced; Liver; Male; Noise; Otoacoustic Emissions, Spontaneous; Oxidation-Reduction; Oxidative Stress; Rats; Reactive Oxygen Species; Thiobarbituric Acid Reactive Substances