Antioxidant metabolism has been examined in red spruce growing at two sites with similar levels of ozone pollution but different winter temperatures. The northern site was Whiteface Mountain, New York with a latitude of 44° 31′(NY). The southern site was Whitetop Mountain, Virginia with a latitude of 36° 54′(VA). The northern site has lower winter temperatures. At the NY site two populations of trees were denned with respect to cold tolerance. An effort was made to establish a temporal relationship between the antioxidant capacity of conifer needles on one hand and the different stages of winter hardening/dehardening, and the induction of dormancy, on the other. The hypothesis tested was that winter injury of red spruce was due to an increased demand for glutathione at levels exceeding the inherent capacity of the needles and/or the altered activities of glutathione reductase.
In the autumn, as temperatures began to decrease, photosynthetic potential decreased as spruce entered dormancy. At the same time, cold tolerance (measured as needle electrolyte leakage) gradually increased. Glutathione metabolism appeared to be coupled to these processes. At both sites, seasonal changes in glutathione levels were observed. These changes were found to coincide temporally with the onset and cessation of dormancy (as measured by decline in photosynthetic activity). The same pattern was observed at the northern and the southern site with the winter increases being greater at the former. Glutathione began to increase as soon as needles entered dormancy and began hardening. Glutathione reductase activities closely followed the dehardening process during spring, while glutathione concentration continued to stay relatively high with prehardening levels reached only by summer. At the northern site during the winter, cold-tolerant trees had significantly higher glutathione reductase activities compared with cold-sensitive ones. Based on these data, it is proposed that individuals that cannot respond to the increased demand for glutathione reductase activity during the hardening, winter and dehardening periods, become susceptible to winter injury.
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