1979 Volume 47 Issue 4 Pages 537-545
The purpose of this experiment is to elucidate the role of L-ascorbic acid (ASA) in the metabolism of phenolic substances, especially in the seed of sweet pepper fruit affected by chilling injury which sometimes takes place under 1°C storage conditions. In the previous paper, two electron transport systems involving ASA were assumed to function in the seed of sweet pepper fruit. One of them (System I) is the electron transport sequence; substrates … G-6-P, GSSG, ASA: coenzyme …NAD: enzyme … G-6-P dehydrogenase … glutathione reductase … dehydroascorbate reductase … ascorbate oxidase; and the other (System II) is the sequence; substrates … ASA, chlorogenic acid, coenzyme … NAD(P)H, enzyme … oxidized ascorbate reductase, polyphenol oxidase.
The present paper deals mainly with the electron transport through the ASA path involved in the respiratory systems of sweet pepper seeds. In addition, time-course changes in functioning of System I and System II during the storage at 1°C was also investigated. The results obtained are summarized as follows:
1. Glutathione reductase and dehydroascorbate reductase which both are supposed to be the components of System I were proved to function actually in the sweet pepper seed. The activity of these enzymes first decreased on the 2nd day of the storage at 1°C and subsequently increased gradually with progress of time.
2. A rapid but consistent oxygen uptake was achieved by both System I and System II. This oxygen uptake remained linear throughout most of the course examined and was fairly inhibited by the application of diethyldithiocarbamate and thiourea. These compounds are known as inhibitors of terminal oxidase, ascorbate oxidase, and polyphenol oxidase which are components of System I and/or System II. These facts may indicate that sweet pepper seeds actually include System I and System II as the parts of their electron transport systems.
3. Oxygen uptake by System I markedly increased after the beginning of the 1°C storage and reached its peak at the time of manifestation of chilling injury, though it gradually decreased thereafter. Oxygen uptake by System II, on the other hand, increased temporarily at the beginning of the storage at 1°C and then decreased sharply with progress of chilling injury.
