Naphthoquinone-induced cataract in mice: Possible involvement of Ca2+ release and calpain activation

N-acetyl-p-benzoquinone imine (NAPQI), a semiquinone metabolite of acetamin ophen, produces cataract in mice. Naphthalene is biotransformed to the cata ractogenic metabolite 1,2-naphtlioquinone (NQ). Intracameral injection of N APQI elicits a rapid increase in free intracellular Ca2+ in the lens epithe lium and calpain activation before lens opacification begins. In order to t est whether the cellular response is a common feature of quinone-induced ca taracts, we injected in this work 1,2-naphthoquinone (NA) in the anterior c hamber of mouse eye and followed cellular responses in the lens prior to op acity development. A marked rise in free intracellular Ca2+ in the lens epi thelium and concurrent activation of calpain were observed within I hr afte r NQ injection preceding lens opacity development. These results support th e suggestion that Call release and calpain activation are involved in the m echanism of quinone-induced cataractogenesis.