Quinolinic acid (QUIN) excitotoxicity is mediated by elevated intracellular Ca 2+ levels, and nitric oxide-mediated oxidative stress, resulting in DNA damage, poly(ADP-ribose) polymerase (PARP) activation, NAD + deple-tion and cell death. We evaluated the effect of a series of polyphenolic compounds [. epigallocatechin gallate (EPCG), catechin hydrate, curcu-min, apigenin, naringenin and gallotannin] with antioxidant properties on QUIN-induced excitotoxicity on primary cultures of human neurons
