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PubMed2000

Halogenated auxins affect microtubules and root elongation in Lactuca sativa.

We studied the effect of 4,4,4-trifluoro-3-(indole-3-)butyric acid (TFIBA), a recently described root growth stimulator, and 5,6-dichloro-indole-3-acetic acid (DCIAA) on growth and microtubule (MT) organization in roots of Lactuca sativa L. DCIAA and indole-3-butyric acid (IBA) inhibited root elongation and depolymerized MTs in the cortex of the elongation zone, inhibited the elongation of stele cells, and promoted xylem maturation. Both auxins caused the plane of cell division to shift from anticlinal to periclinal. In contrast, TFIBA (100 micromolar) promoted elongation of primary roots by 40% and stimulated the elongation of lateral roots, even in the presence of IBA, the microtubular inhibitors oryzalin and taxol, or the auxin transport inhibitor naphthylphthalamic acid. However, TFIBA inhibited the formation of lateral root primordia. Immunostaining showed that TFIBA stabilized MTs orientation perpendicular to the root axis, doubled the cortical cell length, but delayed xylem maturation. The data indicate that the auxin-induced inhibition of elongation and swelling of roots results from reoriented phragmoplasts, the destabilization of MTs in elongating cells, and promotion of vessel formation. In contrast, TFIBA induced promotion of root elongation by enhancing cell length, prolonging transverse MT orientation, delaying cell and xylem maturation.

Biological Transport↗
PubMed1989

Damage to protein synthesis concurrent with lipid peroxidation in rat liver slices: effect of halogenated compounds, peroxides, and vitamin E1.

Protein synthesis and lipid peroxidation were evaluated in rat liver slices incubated in the presence of oxidants and protein synthesis inhibitors. Protein synthesis by rat liver slices was evaluated by [3H]leucine incorporation into the trichloroacetic acid (TCA)-insoluble material, and lipid peroxidation was evaluated by thiobarbituric acid-reactive substances (TBARS) released into the incubation medium. Protein synthesis inhibition by bromotrichloromethane (BrCCl3) or t-butyl hydroperoxide (t-BOOH) depended on the incubation time and oxidant concentration. [3H]Leucine incorporation was decreased to 20 and 47% of control values and TBARS were enhanced from the control value of 16.9 to 45.3 and 62.5 nmol/g of liver by incubation for 1 h with 1 mM BrCCl3 and t-BOOH, respectively. Following incubation, both protein synthesis damage and lipid peroxidation were decreased in control and oxidant-treated slices prepared from rats injected with 200 mg of DL-alpha-tocopherol/kg of body wt. Release of lactate dehydrogenase was not enhanced by oxidant treatment. Protein synthesis inhibitors reversibly decreased [3H]leucine incorporation, but the effect of oxidants on protein synthesis was irreversible. Cumene hydroperoxide and methyl ethyl ketone peroxide, but not hydrogen peroxide, damaged protein synthesis and induced lipid peroxidation. The ability of carbon tetrabromide, benzyl chloride, bromoform, bromobenzene, carbon tetrachloride, chloroform, dichloromethane, and bromochloromethane to inhibit protein synthesis was correlated with their ability to induce lipid peroxidation, and with their LD50. The results suggest that oxidant-induced lipid peroxidation and protein synthesis damage occurred concurrently, and that protein synthesis inhibition may be involved in cell injury or death mediated by free radicals.

Animals↗
PubMed1982

The reductive metabolism of halogenated alkanes by liver microsomal cytochrome P450.

Under anaerobic conditions various polyhalogenated alkanes (CCl3-CCl3, HCl2C-CCl3, CF3-CCl3, CCl4, CF-CHCIBr) stimulate the oxidation of NADPH by liver microsomal fractions. The participation of cytochrome P450 in the NADPH oxidation was shown by inducers and inhibitors of the monooxygenase system. The products of the reductive pathway of hexachloroethane were tetrachloroethene (99.5%) and pentachloroethane (0.5%). From pentachloroethane as substrate trichloroethene (96%) and tetrachloroethane (4%) were produced. The stoichiometry of NADPH oxidation and product formation was close to 1:1. There was a synergistic effect in the presence of NADPH and NADH for both hexa- and pentachloroethane. The influence of dioxygen and radical traps (RSH) on the formation of products from hexachloroethane with reduced cytochrome P450 has been investigated. The results indicate the possibility of a reductive in vivo metabolism of polyhalogenated alkanes even at physiological dioxygen concentrations. For the reductive dehalogenation of polyhalogenated alkanes by microsomal cytochrome P450 a reaction scheme is proposed: the reduction proceeds by two subsequent one electron reductions forming first a radical and then a carbanion. The carbanion can form an alkene via beta-elimination of chloride.

Animals↗