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Fig. 17.6 ALA content, tetrapyrrole accumulation and photodynamic injury in washed
morningglory leaf sections of different ages. The data was adapted from Table 17.6 . All
abbreviations are as in Fig. 17.4 (Reproduced from Kulur 1996 )
The detection of equally small amounts of ALA and lesser amounts of tetrapyrrole
accumulation in older leaves can be explained by several scenarios, none of which is
compatible with a rapid translocation of exogenous ALA to inner tissue. If rapid
translocation of exogenous ALA to inner tissue took place in older leaves, one should
observe one of two phenomena: (a) larger amounts of ALA accumulation, if ALA
conversion to tetrapyrrole is sluggish or (b) larger amount of tetrapyrrole accumula-
tion if ALA conversion to tetrapyrroles is rapid.
Since none of these phenomena were observed in older tissues, two other
scenarios involving a slow translocation of exogenous ALA to inner tissues may
be involved: (a) In one, slow translocation of exogenous ALA to inner tissues is
accompanied also by slow conversion of ALA to tetrapyrroles, or (b) although older
tissues have very active tetrapyrrole biosynthetic capabilities, the very slow trans-
location of exogenous ALA to inner tissue is a limiting factor, that results in poor
tetrapyrrole accumulation.
Distinction between the last two hypotheses is very important since it dictates
how to formulate ALA for field use. In case older tissues exhibit low translocation
rates of exogenous ALA to inner tissues and low conversion rates of ALA to
tetrapyrroles, then ALA formulations should include a TDPH modulator to activate
tetrapyrrole anabolism. On the other hand, in case older tissues exhibit low translo-
cation rates of exogenous ALA to inner tissues, and high conversion rates of ALA
to tetrapyrroles, then ALA formulations that improve the translocation of ALA to
inner tissues should be a focal point. Distinction between these two hypotheses is
carried out in the next experiments described below.
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