Scientific Studies

The purpose of the current study was to evaluate hydrogen-saturated saline protecting intensive narrow band noise-induced hearing loss. 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 (1 ml/100 g) 3 days before and 1 h before narrow band noise exposure (2.5-3.5 kHz 130 dB SPL, 1 h). The guinea pigs in the control group received no treatment. The hearing function was assessed by the auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE) recording. The changes of free radicals in the cochlea before noise exposure, and immediately and 7 days after noise exposure were also examined. By Scanning electron microscopy and succinate dehydrogenase staining, we found that pre-treatment with hydrogen-saturated saline significantly reduced noise-induced hair cell damage and hearing loss. We also found that the malondialdehyde, lipid peroxidation, and hydroxyl levels were significantly lower in the hydrogen-saturated saline group after noise trauma, indicating that hydrogen-saturated saline can decrease the amount of harmful free radicals caused by noise trauma. Our findings suggest that hydrogen-saturated saline is effective in preventing intensive narrow band noise-induced hearing loss through the antioxidant effect.


To explore the effect of saturated hydrogen saline on blue light-induced retinal damage in rats.


The retinal damage of rats was induced by blue light exposure for 6 hours and examined 8 hours, 16 hours and 24 hours after the exposure. One hundred female Sprague-Dawley rats were randomly divided into four groups. Group 1 included 30 rats received light exposure without any other treatment. Group 2 included 30 rats received light exposure with intraperitoneal injection of normal saline. Group 3 included 30 rats received light exposure with intraperitoneal injection of saturated hydrogen saline. And Group 4 included the other 10 rats which did not receive any treatment. The amount of intraperitoneal injection of saturated hydrogen saline and normal saline was calculated in the ratio of 1ml/100g of rat weight. Specimens were collected and processed by H-E staining, ultrastructure observation, biochemical measurement. Morphological changes were observed by light microscope and transmission electron microscope (TEM) and the retinal outer nuclear layer (ONL) thickness was measured by IPP 6.0, while the malondialdehyde (MDA) was measured by colorimetric determination at 532 nm.


Although the structure of retina in Group 1 and Group 2 was injured heavily, the injury in Group 3 was mild. The differences between Group 1 and Group 2 were not significant. Compared with the rats in Group 1 and Group 2, the ones in Group 3 had more clearly demarcated retina structure and more ordered cells by light microscope and TEM observation. The ONL thicknesses (400 times) of four groups at each time point except between Group 1 and Group 2 were significantly different (P❰0.05). The thicknesses of the ONL in Group 1 at three time points were 30.41±4.04µm, 26.11±2.82µm and 20.63±1.06µm, in Group 2 were 31.62±4.54µm, 25.08±3.63µm and 19.07±3.86µm, in Group 3 were 29.75±3.62µm, 28.83±1.97µm and 27.61±1.83µm. In Group 4 the mean of the thickness was 37.35±1.37µm. As time went by, the damage grew more severely. At 24h point, the differences were most significant. Compared with Group 4, the thickness was 46.23% thinner in Group 1, 50.29% thinner in Group 2 and 28.04% thinner in Group 3. The stack structures of membranous disc in Group 3 were injured slightly, but in Group 1 and Group 2 the damage was more obvious by TEM. Compared with Group 4 at each time point, the content of MDA in Group 1 was higher (P❰0.05). The content of MDA in Group 3 was significantly lower than those of Group 1 (P❰0.05) and Group 2 (P❰0.05). Between the Group 1 and Group 2, the MDA concentration at each time point was no significant difference (P>0.05).


Saturated hydrogen saline could protect the retina from light-induced damage by attenuating oxidative stress.


Retinal neovascularization or retinopathy is a proliferative disorder of the retinal capillaries and is the primary cause of blindness. Some studies have shown that oxidative stress plays an important role in hyperoxia-induced retinal neovascularization. Previous reports have indicated that hydrogen has a therapeutic, antioxidant activity by selectively reducing hydroxyl radicals. This study examined the therapeutic effect of hydrogen saline on retinopathy in an established mouse model of hyperoxia-induced retinopathy.


Mouse pups were exposed to 75% O(2) from postnatal day 7 (P7) to P12. Hydrogen saline was administered by intraperitoneal injection (5 ml/kg) daily for 5 days. On P17, the pups were decapitated, and retinal neovascularization was assessed using fluorescence imaging and histopathological examination. Vascular endothelial growth factor (VEGF) expression was evaluated using real-time polymerase chain reaction and fluorescence immunohistochemistry. Oxidative stress was quantified based on the malondialdehyde (MDA) level.


Hydrogen saline decreased retinal neovascularization, reduced the mRNA and protein expression of VEGF, and suppressed the MDA levels.


Hydrogen saline may be a potential treatment for hyperoxia-induced retinopathy that acts via the inhibition of oxidative stress and the reduction of VEGF expression.