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synthetic reductant and A TP are generated in excess of that used in CO 2
assimilation, and that they serve to "replace" the need for some respiratory
metabolism, the resulting reduction in respiration is a benefit to the carbon
and energy balance of a plant. But, a reduction in respiration without
replacement sources of A TP, reductant, and carbon skeletons is likely to be
a detriment to the plant as growth and maintenance processes will be
deprived of substrates.
4.4 Photorespiration and Mitochondrial Metabolism
Mitochondrial glycine decarboxylation and the linked NAD+ reduction is
central to photo respiratory carbon metabolism (Tolbert 1980) with CO2
release by photorespiration probably exceeding that of respiration under
moderate to high light and ambient CO2. Reduction of mitochondrial NAD+
(forming NADH + H+) by glycine decarboxylase could deprive NADlinked TCA cycle dehydrogenases of that co substrate and limit TCA cycle
activity. Moreover, a supply (regeneration) of NAD+ is required for photorespiration as well as TCA cycle activity. If carbon flux through the photorespiratory cycle does not match and rate of RuP2 oxygenation, which is a
function of chloroplast CO2 and O2 partial pressures and the temperaturedependent substrate specificity of Rubisco (Jordan and Ogren 1984), photosynthesis is slowed (Dry et al. 1987). The fate of mitochondrial NADH
during daytime is therefore important to rates of respiration, photorespiration, and photosynthesis.
4.4.1 Oxidation of Photo respiratory NADH by the Respiratory Chain
Matrix NADH formed by glycine decarboxylase (Fig. 4.6) can be oxidized
by the mitochondrial respiratory chain and coupled to as many as three sites
of proton translation (Douce 1985; Fig. 4.3), but that oxidation might
compete with TCA cycle-generated NADH and succinate for access to the
UQ pool. Photo respiratory NAD+ reduction might elicit rotenone-resistant
complex I bypass activity because of high matrix NADH levels and also
enhance alternative pathway engagement due to increased reduction of the
UQ pool. Dry et al. (1987), however, consider the latter to be relatively
unimportant to normal daytime activity of the respiratory chain.
Glycine may have preferential access to some mitochondrial NAD+, or
the resulting NADH may have preferential access to the respiratory chain,
compared to NAD+-linked TCA cycle enzymes and the NADH formed by
them. Glycine decarboxylation will not saturate the respiratory chain however, for when a second substrate such as malate is added to mitochondria
supplied with glycine, O2 uptake can increase markedly (Dry et al. 1987;
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