Accumulation of glutathione in pea leaf discs exposed to the photooxidative herbicides acifluorfen and 5-aminolevulinic acid

Factors controlling the increase of glutathione (GSH) level by the photooxidative herbicides acifluorfen and 5-aminolevulinic acid (ALA) were studied in pea leaf discs. Light intensity had a significant influence on the induction of GSH by both photooxidative agents. Levulinic acid, the known inhibitor of chlorophyll biosynthesis, only partially prevented the induction of GSH by acifluorfen, but completely blocked the effect of ALA. The increase of GSH level by acifluorfen could be completely prevented by L-buthionine-[S,R]-sulfoximine (BSO), which is an inhibitor of GSH biosynthesis. The GSH precursor L-2-oxo-4-thiazolidine-carboxylic acid (OTC) strongly elevated the GSH level in pea leaf discs, but no synergistic effect was found when acifluorfen and OTC were applied together. The known inhibitor of glutathione reductase (GR) activity in mammalian tissues, 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU), was also shown to inhibit pea leaf GR activity in vitro, and to a lesser extent also in vivo. In contrast to BSO, BCNU treatments did not decrease the GSH accumulation caused by acifluorfen. The modulation of the cellular GSH level by BSO, BCNU and OTC did not significantly modify the toxic effect of acifluorfen exerted on the photosynthetic activity of pea leaf discs.