Retardation of ultraviolet light accelerated chlorosis by visible light or by benzyladenine in nicotiana glutinosa leaves: changes in amino acid content and chloroplast ultrastructure.

Abstract

Abstract— Low doses (180–720 Jm‐2) of ultraviolet light (254 nm) are known to accelerate the chlorosis of detached leaves in darkness. The development of such chlorosis is prevented by a photoreactivation treatment. However, we found that delayed light exposure or benzyladenine treatments (which were not effective in photorepair of UV‐induced thymine dimers in cell DNA) were also effective in retarding the UV‐accelerated chlorosis.Small drops of benzyladenine solution placed on the UV irradiated leaf formed green islands which acted as strong sinks for the accumulation of free amino acids during dark incubation. To a lesser degree, non–irradiated green tissues surrounded by irradiated yellow leaf tissue also acted as sinks for amino acid accumulation.The accelerated chlorophyll loss in UV‐irradiated leaves was correlated with degradation of chloroplast ultrastructure. Visible light or benzyladenine retarded this chloroplast degradation. The accelerated senescence of UV irradiated leaf tissue, therefore, is ultrastructurally and physiologically similar to normal senescence of detached dark‐incubated leaves, but progresses at a faster rate.When the lower leaf surface was irradiated with high UV doses (3600–10,800 Jm‐2), the chloroplast ultrastructure of the spongy cells (except the envelope) was preserved for 3 days after dark incubation. However, the chloroplasts of the palisade cells were in a late stage of senescence. Since the spongy cells were dead (plasmalemma, tonoplast and chloroplast envelope disappeared), the maintenance of green color and ultrastructure of chloroplasts could have been due to inhibition of degrading enzymes normally associated with senescence.