Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:6.2.1.7 (
BAL
)
1,977
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
BAL
(2,3-dithiopropan-1-ol) treatment of chloroplasts has previously been reported to induce a block in electron transport from water to
NADP+
at a site preceding plastocyanin [Belkin et al. (1980) Biochim. Biophys. Acta 766, 563-569]. In the present work the block was further characterized. The following properties of
BAL
treatment are described. Inhibition of electron transport from water to lipophilic acceptors but not to silicomolybdate. Inhibition of the slow, sigmoidal phase of chlorophyll a fluorescence induction. Inability of N,N,N',N',-tetramethyl-p-phenylenediamine to bypass the inhibition of
NADP+
photoreduction with water as the electron donor. Inhibition of electron transport from externally added quinols to
NADP+
. Inhibition of cytochrome f reduction by photosystem II, but not its oxidation by photosystem I. Inhibition of cytochrome b6 turnover and cytochrome f rereduction after single-turnover flash illumination under cyclic electron-flow conditions. The
BAL
-induced block is therefore located between the secondary quinone acceptor (QB) and the cytochrome b6f complex. It was further found that (a) the isolated cytochrome complex is not inhibited after
BAL
treatment; (b)
BAL
-reacted plastoquinone-1 inhibits electron transport in chloroplasts; (c)
BAL
does not inhibit electron transport in chromatophores of Rhodospirilum rubrum or Rhodopseudomonas capsulata. It is suggested that the inhibition of electron transport in chloroplasts results from specific reaction of
BAL
with the endogenous plastoquinone.
...
PMID:The site of inhibition of the chloroplast electron-transport system by 2,3-dithiopropan-1-ol (BAL). 356 75
