Int. J. Environ. Res. Public Health 2010, 7 3732 region on the mouse chromosome 17 and its role in NIHL. They found a resistance to NIHL after prolonged noise exposure in mice when the wild type Ahl3 allele was present, demonstrating a genetic variation in susceptibility to NIHL. Hearing loss from otologic trauma, which is defined as a sudden change in hearing due to exposure of a sudden burst of sound, may be due to a different mechanism of action than NIHL, and should be thought of as a separate entity. Acoustic trauma can cause mechanical disruption of the cochlea and may result in permanent hearing loss. In 1944, Lurie et al. [16] described graduated degrees of acoustic trauma in guinea pigs beginning with stripping of mesothelial cells under the basilar membrane, progressing to disruption of external hair cells and eventually, separation of the Organ of Corti from the basilar membrane as the time of exposure increased. Noise induced hearing loss, on the other hand, is thought to be due to various other mechanisms. One leading theory that will be focused on in this article is the role of oxidative stress in chronic noise exposure. Oxidative Stress Pathology arising from increased metabolic activity in the inner ear was originally proposed by Lim and Melnick (1971) [17] and gained popularity with work by Yamane in 1995 [18,19]. Presently, there is an abundance of literature exploring the role of oxidative stress in NIHL [20,21]. Exposure to noise has been demonstrated to cause an initial increase in cochlear blood flow. Within a short period of time, there is an abrupt decrease in cochlear circulation seen by an aggregation of RBCs, capillary vasoconstriction, and stasis [22]. This intense metabolic activity and decreased cochlear blood flow from noise exposure alters cellular redox states and drives the formation of free radicals [23]. These free radicals may also be generated by a variety of mechanisms. They may form invivo as a byproduct of mitochondrial respiration, called Reactive Oxygen Species (ROS), arise from environmental contaminants, or can be produced from ionizing and ultraviolet radiation [21]. ROS include the superoxide ion (O2−), hydrogen peroxide (H2O2), and the hydroxyl radical (OH−), hypochlorite (OCl−), and nitric oxide (NO−) to name a few. In excess, ROS can damage cellular DNA, proteins, and lipids, as well as up regulate apoptotic pathways causing cell death and irreparable damage to eloquent hearing structures [24]. Research on oxidative stress has spawned subsequent attention toward the protective role of antioxidants in NIHL. The senior author has published multiple studies on the role of anti-oxidants in protection against NIHL. One of these studies evaluated the effects of resveratrol on NIHL. Resveratrol is a substance found in the skin of grapes and over 70 other fruits and plants. It has many beneficial biological properties that include inhibiting lipid peroxidation, free-radical scavenging, anti-inflammatory activity, inhibiting platelet aggregation, vaso-relaxing activity, anti-cancer properties, and cardio-protection to name a few [25-27]. In this 2003 study by Seidman et al., Fischer rats were randomized into a treatment and control group. The treatment group was pretreated for 3 weeks with resveratrol solution (430/ug/kg/day) prior to a 24-hour exposure to a 105 dB noise at 4,500 to 9,000 Hz. The treatment group were then given four weeks of post-stimulus treatment while the control group received only saline. The results from this study demonstrated a significant reduction of auditory threshold shifts in the treatment group compared to the controls. There was also a decrease in the loss of hair cells in the Organ of Corti in the treatment group compared to the control group.