QUIN toxicity | References | Aβ toxicity | References |
---|---|---|---|
• Free radical production via over-activation of NMDA receptor and/or QUIN-Fe2+ complexes and consequent lipid peroxidation and cell death. | (Platenik et al., 2001) (Stone and Perkins, 1981) | • Free radical production via Fenton reaction by metals Cu and Fe and consequent lipid peroxidation and apoptosis. | (Huang et al., 1999) (Varadarajan et al., 2001) (Markesbery and Lovell, 1998) (Tamaoka et al., 2000) |
• Excessive PARP activation leading to NAD depletion. | (Maldonado et al., 2007) | • DNA damage by ROS leads to PARP over-activation and NAD depletion. | (Meyer et al., 2006) (Love et al., 1999) |
• Activation of astrocytes including release of inflammatory chemokines and astrogliosis. | (Guillemin et al., 2003b) (Dihne et al., 2001) (Hanbury et al., 2002) | • Activation of microglia and other immune cells leading to secretion of inflammatory cytokines and proteins. • Co-activation of astrocytes by inflammatory factors leading to further release of cytokines and astrogliosis. | Griffin and Mrak, 2002) (Murphy et al., 1998) (Selmaj et al., 1990) |
• Inhibition of glutamate uptake leading to excitotoxicity. | (Tavares et al., 2002) | • Aβ can increase extracellular glutamate resulting in NMDA receptor over-activation and excitotoxicity. | (Lafon-Cazal et al., 1993; Keller et al., 1997; Lauderback et al., 2001) (Harris et al., 1995; Harris et al., 1996) |
• NMDA receptor activation by QUIN can lead to Aβ production. | (Lesne et al., 2005) | • Aβ can induce IDO in the KP and increase production of QUIN. | (Guillemin et al., 2003a) |