Plant Mitochondrial Respiration Under the Influence of Heavy Metals

Abstract

7.1 INTRODUCTION Cell respiration like other metabolic processes is catalysed by many enzymes that require metals as cofactors, whereas higher concentrations of these metals and other non-essential metals inhibit enzyme activity. Enzymes of dissimilation processes are less affected by higher doses of heavy metals than the enzymes of the energy fixation and carbon assimilation pathways (van Assche and Clijsters 1990). This may be one reason why the majority of research on heavy metal physiology is more concentrated on processes of metal exclusion from the symplast and metal sequestration in the vacuole (e.g. Ernst 1969, 1976; Denny and Wilkins 1987; Hall 2002), on metal toxicity effects on photosynthesis (e.g. Vallee and Ulmer 1972; Clijsters and van Assche 1985), and in particular on metal interactions with gene expression (e.g. Tomsett and Thurman 1988; Cobbett 2000; Clemens 2001). Despite progress in knowledge in all these fields, lack of detailed insight into heavy metal interactions with metabolic processes still hinders a complete causal understanding of toxicity and tolerance mechanisms (e.g. Foy et al. 1978a; Jackson et al. 1990; Mukhopadhyay and Sharma 1991; Barcel6 and Poschenrieder 1992), and this statement is particularly true for plant respiration. Heavy metal effects on mitochondrial respiration-photorespiration is not considered in this chapter-become obvious by changed 02 consumption rates and altered amounts of CO 2 release from metal-treated plants. At the biochemical level heavy metal disturbances of the catabolic pathways result in lowered ATP production and changed amounts of intermediate substances, e.g. of the citrate cycle. Respiration rates remain unchanged or even increase if sensitive organelles in the symplast remain protected from the ionic stressor due to metal exclusion or sequestration in the vacuole. The increase in respiration rates can be a consequence of an increased M.