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The impact of heat shock on minimising the activity of photosystem 2 (PS2) initiating high lipid peroxidation (POL) level and consequently changes in the enzymatic-antioxidant protective system was studied in seedlings of two Egyptian cultivars of barley (Giza 124 and 125). Heat doses (35 and 45 °C for 2, 4, 6, and 8 h) decreased chlorophyll (Chl) contents coupled with an increase in Chl a/b ratio, diminished Hill reaction activity, and quenched Chl a fluorescence emission spectra. These parameters reflect the disturbance of the structure, composition, and function of the photosynthetic apparatus as well as the activity of PS2. POL level, as dependent on the balance between pro-and anti-oxidant systems, was directly correlated with temperature, exposure time, and their interaction. Heat shock caused an increase in the electric conductivity of cell membrane, and malonyldialdehyde content (a peroxidation product) coupled with the disappearance of the polyunsaturated linolenic acid (C 18:3 ), reflecting the peroxidation of membrane lipids which led to the loss of membrane selective permeability. Moreover, it induced distinct and significant changes in activities of antioxidant enzymes. Superoxide dismutase and peroxidase activities have been progressively enhanced by moderate and elevated heat doses, but the most elevated one (45 °C for 8 h) showed a decrease in activities of both enzymes. In contrast, catalase activity was reduced with all heat shocks.

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In this paper, we show the unique role of bicarbonate ion in stimulating the electron transfer of photosystem II (PS II) in formate-treated leaf discs from spinach. This is referred to as the "bicarbonate effect" and is independent of the role of CO2 in CO2 fixation. It is shown to have two sites of action: (1) the first, described here for the first time, stimulates the electron flow between the hydroxylamine donation site ("Z" or "D") and QA, the first plastoquinone electron acceptor and (2) the other accelerates the electron flow beyond QA, perhaps at the QA QB complex, where QB is the second plastoquinone electron acceptor. The first site of inhibition by formate-treatment is detected by the decrease of the rate of oxygen evolution and the simultaneous quenching of the variable chlorophyll a (Chl a) fluorescence of leaf discs infiltrated with 100 mM formate for about 10 s followed by storage for 10 min in dark. This is referred to as short-term formate treatment. Addition of bicarbonate reverses this short-term formate effect and restores fully both Chl a fluorescence and oxygen evolution rate. Reversible quenching of variable Chl a fluorescence of heated and short-term formate treated leaf discs, in the presence of hydroxylamine as an artificial electron donor to PS II, is also observed. This suggests that the first site of action of the anion effect is indeed between the site of donation of hydroxylamine to PS II (i.e. "Z" or "D") and QA. The second site of the effect, where bicarbonate depletion has its most dramatic effect, as well known in thylakoids, is shown by an increase of Chl a fluorescence of leaf discs infiltrated with 100 mM formate for about 10 min followed by storage for 10 min in dark. This is referred to as the long-term formate treatment. Addition of bicarbonate fully restores the variable Chl a fluorescence of these leaf discs. Chl a fluorescence transient of DCMU-infiltrated (10 min) leaf discs is similar to that of long-term formate-treated one suggesting that the absence of bicarbonate, like the presence of DCMU, inhibits the electron flow beyond QA.