Background: Occupational noise exposure is one of the leading factors for developing noise-induced hearing loss (NIHL), particularly among workers worldwide. The literature review reveals that beside conventional strategies for preventing NIHL, multiple interventions can be applied to reduce or prevent such disorders. The present study aimed to investigate the preventive effects of normobaric hyperoxia pre-and post-treatment on the development of NIHL in rats. Methods: Four groups of male Wistar rats were exposed to pure oxygen alone, noise alone, or oxygen plus noise for 6 hours a day, 5 days a week for 4 weeks. One group served as the control and received neither noise nor oxygen. Animals in the noise groups were exposed to high-pass white noise of 100 dB SPL, centred at 8 KHz. The treatment protocols were based on inhalation of pure normobaric oxygen (95%) for 3 hours in a chamber either before or after noise exposure. The auditory brainstem responses (ABRs) for click and 4, 6, 8, 12, and 16 kHz stimuli, as well as distortion product otoacoustic emissions (DPOAEs) at 4, 6, 8, and 10 kHz, were recorded to assess the level of hearing impairment before exposure and 4 weeks post-exposure. Results:The results showed that pre-treatment of rats with 3 hours of normobaric hyperoxia contributed to a significant reduction in ABR threshold shifts, while improving the DPOAE amplitudes (P < 0.01). However, three hours of post-treatment did not produce any comparable results in terms of ABR threshold shifts or DPOAE amplitude improvements. DPOAE amplitudes and ABR threshold shifts remained almost constant during exposure in the control group (P > 0.05). Conclusions: Pre-and post-treatment with normobaric hyperoxia seem to produce protective effects through either boosting cellular oxygenation or maximizing antioxidant enzyme activities and tolerance against noise-induced ischemia and hypoxia in the cochlea. Therefore, application of normobaric hyperoxia pre-or post-treatment, along with other conventional protective strategies, can be helpful in the fight against NIHL.

No abstract

The purpose of this study was a complementary method to the diagnosis and prognosis of complete hydatidiform mole (CHM) and differentiate it from the other cases of gestational trophoblatic diseases. This was done by examining the quality and quantity of the total and the placental alkaline phosphatase activity. The ALP in the tissues and sera from 12 patients were compared with 13 control normal non-pregnant and 30 control pregnant females. The enzyme activities were determined by biochemical and histochemical examination. The placental tissues were obtained from uterine curettage, or after delivery which then were frozen in a liquid nitrogen and processed for biochemical study. Cryosections were histochemically stained for ALP and PLAP by the azo coupling method. Isoenzyme specificity was evaluated by heating the tissue at 65 degrees C for 15 min while the including L-phenylalanine (50 mM), D-phenylalanine (50 mM) and L-homoarginine (50 mM) were used for chemical inhibition study. The activity of ALP and PLAP of patients were reduced in comparison with pregnant control group (P<0.05). There was no significant difference between the patients and non-pregnant control (P<0.05) group. The localization of enzyme activities in cryosections of all groups were in the basal, apical, and the cytoplasm of syncytiotrophoblast cells. The ALP in all the groups was thermostable (65 degrees C for 15 min) and was inhibited by L-phenylalanine, but no inhibition was seen with L homoarginine in patients group only. These findings suggest that the PLAP is a useful marker in the diagnosis and prognosis of hydatidiform mole.