Abstract

The shoots of 16-day-old spring wheat plants (Triticum aestivumL., cv. Albidum 29) were subjected to heat shock (HS) at 40, 41, or 43°C for 10 min. The activity of the Hill reaction in chloroplasts isolated immediately after HS was 83, 61, and 30% of the initial value, respectively. The activity of the Hill reaction was also estimated after plant return to the initial growth conditions for one day. It was completely restored after heating at 40°C and achieved 82 and 30–33% of the initial level after heating at 41 and 43°C, respectively. Thereafter, the shoots were heated repeatedly at 42, 43, or 43.5°C for 10 min, and the activity of the Hill reaction was measured immediately or one day after this heating. Immediately after the second heating, the activity decreased again as compared to its value before heating. The percent of inhibition of the Hill reaction was similar in the control plants not subjected to preliminary HS and HS-treated plants independently of the temperature used. However, after one-day growth under normal conditions, the activity of the Hill reaction was restored almost completely in HS-treated plants but not more than by 10% in the control plants. The conclusion is that different mechanisms underlie the development of the tolerance to HS and recovery. Some plants were tested for the effect of HS (40°C) on their tolerance to photoinhibition. The degree of the Hill reaction inhibition after plant exposure to the light of 65–75 klx for 3 h was essentially similar in detached leaves from the HS-treated and unheated plants and comprised about 40% of the activity before light stress. After the leaves were returned to the low-light conditions for 3 h, the Hill reaction was restored and attained about 75% of that before photoinhibition in both HS-treated and untreated plants. The lack of the HS-induced stimulation of the Hill reaction recovery after photoinhibition is evidently related to the fact that heating and excess light damage different sites of photosystem II, which implies the different pathways for the recovery of its functional activity.

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