Effect of Orally Administered Glutathione Peroxidase Mimetic towards Glutathione and Malondialdehyde Blood Level and Otoacoustic Emissions Result in Soldiers with Acoustic Trauma Risk Caused by Howitzer 105 Artillery Weapon BLAST

Excessive noise exposure may cause mechanical and metabolic (oxidative stress) to the inner ear structure (cochlea), resulting in acoustic trauma (TA). Oxidative stress which caused by increasing of free radical ROS/RNS in the organs of Corti, causing apoptosis and necrosis of cochlear hair cell. Oxidative stress was characterized by increasing of malondialdehyde (MDA), decreasing of glutathione peroxidase (GPx) enzyme, and abnormal otoacoustic emission value (refer). Defense mechanism toward oxidative stress was mediated by endogenous antioxidant enyzme (superoxide dismutase/SOD, catalase/CAT, and GPx). Cellular mechanism of glutation peroxidase mimetic was similar as GPx.    Aim of this study was to determine the impact of glutathione peroxidase mimetic to glutathione peroxidase and malondialdehyde level in blood, also otoacoustic emission value on soldiers with risk of TA due to explosion of Howitzer 105 artillery weapon. The design of this study was clinical trial pre and post design, randomized, double blind and placebo controlled, on 34 new recruit soldiers in Artillery Academy of Indonesian Army, during the soldiers were trained to firing Howitzer 105 artillery weapon, from 7th-10th July 2014 in Cimahi and Batujajar. Subjects were divided into 2 groups, the exposure group (group given treatment) and control group. Exposure group was given glutathione peroxidase mimetic (Ebselen SPI 1005) 200mg, orally once daily during the training, meanwhile control group was given. Malondialdehyde and Glutathione Peroxidase level in blood, pure tone audiometry and otoacoustic emission value (DPOAEs) was measured from those two groups, before and after firing training. The data was analyzed using parametric and non parametric, with Number Needed to Treat (NNT, 95%CI) and significance value (p