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Several mutations in Cu, Zn-SOD gene are found to be associated with FALS.[66] In addition, Cu, Zn-SOD is one of the prime victims of oxidative damage to the brain in AD and Parkinsons disease.[67] It has been experimentally demonstrated that overexpression of SOD-2 reduces hippocampal superoxide and hence prevents memory deficits in a mouse model of AD.[68] SOD supplementation showed improvement in mice model of AD.[69] SOD/catalase mimetic EUK-207 exhibited protection against and interruption of progression of amyloid and tau pathology and cognitive decline in a mouse model of AD.[70] SOD and diabetes Increased oxidative stress plays a major role in the etiology of diabetes and its complications.[71-73] In diabetes, persistent hyperglycemia stimulates the production of ROS from various sources.[74] As a result, diabetes usually leads to increased formation of ROS and weakened antioxidant defenses.[75,76] SOD catalyzes the conversion of O 2 - into H 2 O 2

FIGURE 3 Protection Against AQ-QI- and DEAQ-QI-Induced Apoptosis by GSTP1 To test whether AQ-QI and DEAQ-QI exposure induced apoptosis and to study the protective potential of GSTP1, activity of caspase 3 was measured under normal and GSH-depleted conditions ( Figure 4 )

(A) TIDE analysis of GSS , SRM and HMBS CRISPR/Cas9 knockouts in TaC12 and BoMac cells

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