Potassium cyanide (KCN)-induced hypoxia is considered under the histotoxic hypoxia associated with oxydative stress and subsequent peroxidation of liqid mambrane in neuronal models (Gunasekar et al., 1996; Johnson et al., 1987; Muller and Krieglstein, 1995). In addition to increased production of ROS and NO, cyanide inhibits brain antioxydant defense that predisposes to oxidative injury (Ardelt et al., 1989; Gunasekar et al., 1996). As a result, the nervous system is exposed to the risk to chemical hypoxia-induced cytotoxicity. In comparison to other cells of the body, neurons are more vulnerable to ROS damage. Mounting report has implicated the role of ROS in the neurodegenerative diseases like parkinsson desease, and Alzheimer’s disease (Simonian and Coyle, 1996). It is well documented that ROS may play an important role in the processes leading to neuronal cell damage to hypoxia (Ratan et al., 1994) but precise mechanism by which degeneration occurs is still not fully known. Bossenmeyer et al. had shown that cultured rat brain neurons on exposure to hypoxia/reoxygenation induce apoptosis (Bossenmeyer et al., 1998).
In present study, we explore the antioxidant capacity of flovonoids especially quercetin (structure shown in Fig. 3) to investigate their neuroprotective ability against KCN-induced chemical hypoxia (Pavlakovid and Eyer, 1995). quercetin is a plant-derived flavonoid, which is used as a nutritional supplement. It is well documented that quercetin have antyinflammatory and antioxidant properties and it is being investigated for a wide range of potential health benefits.