Introduction: bleaching herbicides

Many structurally unrelated bleaching herbicides cause either white or yellow chlorosis of leaves, which is obviously a consequence of the total or partial absence of the normal chloroplast pigments, i.e. chlorophylls and carotenoids. The chlorosis may result from the inhibition of pigment biosynthesis or from the destruction of existing pigment. As a general rule, biosynthesis inhibitors only give rise to chlorosis in newly developing leaves, and are most effective as herbicides when given as a pre-emergence treatment. On the other and, the inhibition of photosynthesis and photosynthetic electron transport by other herbicides frequently leads to the destruction of existing chloroplast pigments. Although this chapter is intended primarily to discuss the inhibitory effects of herbicides on pigment biosynthesis, these effects can be difficult to distinguish from pigment destruction.

Chlorophylls and carotenoids in photosynthesis

To appreciate the importance of pigment biosynthesis as a target for herbicide activity it is necessary to understand the fundamental roles that the pigments play in normal photosynthesis. The chlorophylls and carotenoids are located specifically in the pigment–protein complexes (PPC) within the thylakoid membranes. Each functional PPC has its own distinctive pigment composition. Thus the reaction centre core complexes of photosystems I and II (PSI and II) have chlorophyll α and are enriched in β-carotene whereas the light-harvesting chlorophyll-proteins (LHCP) associated with PSI and PSII contain both chlorophylls a and b together with the xanthophylls, Iutein, violaxanthin and neoxanthin (Siefermann-Harms, 1985).