LIPID-PEROXIDATION AND SUPEROXIDE PRODUCTION IN COWPEA (VIGNA-UNGUICULATA) LEAVES INFECTED WITH TOBACCO RINGSPOT VIRUS OR SOUTHERN BEAN MOSAIC-VIRUS

The role of lipid peroxidation during virus-induced necrotic hypersensitive reaction and nonnecrotic infection was studied in cowpea (Vigna unguiculata) leaves infectcd, respectively, with tobacco ringspot virus (TRSV) and southern bean mosaic virus-cowpea strain (SBMV). In TRSV-infected tissue, increased lipid peroxidation was detected 12 h prior to any significant potassium efflux and 9 h before local lesion appearance. Lipid peroxidation increased during lesion development, declining at 72 h after infection, the time of tissue collapse. Elevated superoxide production and superoxide dismutase activity paralleled the increase in lipid peroxidation. Lesion production was inhibited by pretreatment with superoxide dismutase or the Tree radical scavengers AET (2-aminocthylisothiouronium bromide hydrobromide) and Tiron (4,5-dihydroxyr'l,3-bcnzenedisulphonic acid). In nonnecrotic SBMV infection, levels of lipid peroxidation were lower than those in the TRSV-infectcd plants, but above those of the control tissue. Lipoxygenase and catalase activities were not different from the control in either the necrotic or the nonnecrotic infections. While lipid peroxidation in virus-induced hypersensitive reaction appears to be a critical component of symptom development, it may result from the virus-induced accelerated senescence during nonnecrotic infection. © 1993 Academic Press, Inc.