Abstract

Low temperatures severely limit photosynthesis and growth of chilling-sensitive species. The decrease in photosynthetic capacity may be partly due to chilling-associated oxidative damage to chloroplast components. Thus, we sought to determine the extent of lipid peroxidation and oxidative damage to thylakoid proteins in leaves of soybean (Glycine max L. Merr.) exposed to chilling stress under light. The ratio of variable to maximum fluorescence (Fv/Fm) decreased in plants exposed for 24 h to 7 °C and 500 μmol m−2 s−1 of photosynthetic photon flux density (PPFD), but not in leaves chilled in darkness. The initial drop in Fv/Fm was exacerbated by treatment with the chloroplast protein synthesis inhibitor lincomycin, suggesting that concurrent repair ameliorated chilling-associated damage to photosystem II (PSII). The degree of oxidative damage to thylakoid proteins (i.e., carbonylation) and lipids (estimated as malondialdehyde content) did not change in response to chilling. Likewise, exogenous applications of the ascorbic acid precursor l-galactono-1,4-lactone (Gal) or of the α-tocopherol analog 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid (Trolox) did not prevent the chilling-induced decrease of Fv/Fm, although they were effective in protecting thylakoids from oxidative damage caused by paraquat. Our data suggest that chilling stress does not cause rampant oxidative damage to thylakoid proteins and lipids, and that other cell compartments may be more susceptible than thylakoids to oxidative damage associated with low temperature stress.

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