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Dibutylchloromethyltin chloride, a potent inhibitor of electron transport in plant mitochondria.

Dibutylchloromethyl tin chloride (DBCT) inhibits coupled and uncoupled respiration of mitochondria from potato tubers, cauliflower florets and etiolated mung bean hypocotyls with succinate and L-malate but not with external NADH or TMPD/ascorbate as substrates. Using potato and cauliflower mitochondria. DBCT at 200 pmole/mg of protein gives complete inhibition only in KCl-based media and at pH 6.8. DBCT has no effect on the internal pH of mung bean mitochondria, but does cause a decrease in the membrane potential. Electron transport through the alternative oxidase is not inhibited, neither is the ATP-synthase system. DBCT appears to interact with the functionally-distinct pool of ubiquinone associated with the oxidation of succinate and L-malate.

Electron Transport↗

Interaction of photosystem I-derived protons with the water-splitting enzyme complex. Evidence for localized domains.

The induction of millisecond delayed fluorescence mediated by PS I-dependent proton pumping has been used as an indicator of the time course with which those protons equilibrate with sites on the oxygen-evolving enzyme complex (Bowes, J. M., and Crofts, A. R. (1978). Z. Naturforsch. 33C, 271-275). We found that the induction curves were retarded by a reversible exposure of non-energized thylakoids to low concentrations of the uncoupler, desaspidin, at alkaline, but not at neutral, pH. The induction curves were not retarded by increasing the buffering capacity of the thylakoid lumen with Tricine, and were inhibited by the energy transfer inhibitors, dicyclohexylcarbodiimide (DCCD) and triphenyltin chloride (TPT). These data suggest that the catalytic site of the water-splitting complex is located in proton-sequestering membrane domains, rather than at the lumen-exposed inner membrane surface, protons released during PS I-mediated electron transport might equilibrate with protonatable sites on the oxygen-evolving complex without passing through the lumen, and those protons may travel over specific conducting pathways which can be blocked by DCCD and TPT.

Chlorophyll↗

Inhibition of oxidative metabolism in rabbit polymorphonuclear leukocytes by triphenyltin chloride.

Treatment of rabbit polymorphonuclear leukocytes (PMN) with triphenyltin chloride (TPTCl) inhibited chemiluminescence generation stimulated by particulate stimulus, zymosan, or soluble stimuli, concanavalin A + cytochalasin D. Superoxide anion (O-2) production was also inhibited, indicating that the inhibition involved inhibition of early oxidative metabolic process(es). The direct inhibition of the activation process of the oxidative burst was established by the experiments showing that a) chemiluminescence generated by xanthine oxidase-acetaldehyde system was not inhibited by TPTCl, b) washing the PMN after the treatment with TPTCl did not affect the results of chemiluminescence, and c) there was no change in cell viability after the treatment with TPTCl.

Animals↗

The role of electrogenic pump in Chara corallina.

The conductance, G, and the electromotive force, E, of the Chara membrane were determined accurately by using the current-clamp technique. The measurements at the final steady state of inhibitor poisoning give the conductance, g1, and the electromotive force, E1, of the passive ion conducting pathways. By knowing these values the conductance, g2, and the electromotive force, E2, of the electrogenic pump can be calculated from the measured G and E at each time during the progress of inhibitor poisoning. The local closed circuit current, i, which usually causes a hyperpolarization across the passive conducting pathways, can be calculated by using g1, g2, E1 and E2 thus determined. The values of g2 and i decrease monotonically to zero with the progress of poisoning, while E2 approaches E1 asymptotically after a transient hyperpolarization. During excitation i increases markedly. Such an increased inward current through the passive conducting pathways may help in accelerating the inactivation of the excitatory mechanism.

Action Potentials↗

Species difference in sensitivity to the diabetogenic action of triphenyltin hydroxide.

The sensitivity to the diabetogenic action of triphenyltin hydroxide (TPTOH) was investigated in 5 species of experimental animals. A single oral administration of TPTOH produced marked hyperglycemia and triglyceridemia in rabbits and hamsters, but no evidence of diabetes was found in mice, rats and guinea-pigs. No morphological abnormality was observed in islet tissue from TPTOH-treated hamsters.

Animals↗

Effect of triphenyltin chloride on the release of histamine from mast cells.

The effects of triphenyltin chloride (TPTC) on the release of histamine from rat and mouse mast cells in vitro and in vivo were investigated. The results obtained are summarized as follows: (a) At doses between 1 and 3 mg/kg, TPTC inhibited the dye leakage due to passive cutaneous anaphylaxis mediated by IgE antibody in mouse ear. At the same doses, TPTC inhibited the swelling due to reversed cutaneous anaphylaxis mediated by IgG antibody in rat. However, TPTC did not affect dye leakage due to histamine, serotonin, and LTC4 in rat skin; (b) Histamine release by antigen and IgE antibody in rat peritoneal cavity was inhibited by the administration of TPTC at doses between 0.3 and 3 mg/kg; (c) Histamine release by calcium ionophore A 23187 from purified rat peritoneal mast cells in vitro was inhibited by TPTC at concentrations between 10(-7) and 10(-6) M. At the same concentration, TPTC, itself, caused neither the release of histamine nor any change in cell viability which was supported by the activity of lactate dehydrogenase (LDH) from purified rat peritoneal mast cells. All this evidence suggests that TPTC has an inhibitory effect on the release of histamine from mast cells without direct cytotoxicity.

Animals↗

Effect of Brestan on Saccharomyces cerevisiae during continuous cultivation.

An increase in Brestan concentration in nutrient media decreased the content of protein, phosphorus, total ribonucleic acid, activity of pyruvate carboxylase and isocitrate lyase in cells of Saccharomyces cerevisiae parent strain and respiratory deficient (RD) mutant while the trehalose content increased. The respiration quotient value for the RD mutant was higher than for the parent strain. The RD mutant lacked cytochrome aa3; cytochrome c and b contents were lower than those of the parent strain.

Cytochromes↗