Hydrogen Peroxide Appears to Mediate a Decrease in Hydraulic Conductivity in Wheat Roots under Salt Stress

Changes in the root diameter were measured in wheat, Triticum aestivum L., using a sensor of small displacements in osmotic experiments, and the hydraulic conductivity (L _p) of the root was calculated by the method of initial flows. The L _p decreased by two to three times during 30-min exposure in 0.1–9 mM H₂O₂. In 150 mM NaCl, changes in L _p exhibited two-phase kinetics: an initial increase in L _p by two and a half to three times, followed by a decrease to 1.6–50% of the control level within the subsequent 24 h. After one-day-long exposure of the roots in a solution containing 150 mM NaCl and 100 mg/l catalase, L _p did not differ from the control level. Root pretreatment with salicylate, which promotes the formation of H₂O₂, prevented the initial increase in L _p in 150 mM NaCl, probably, due to a drastic L _p decrease. The activity of guaiacol peroxidase in the roots increased by three times within the 20-min exposure of the roots to the salt solution. The data suggest that hydrogen peroxide can mediate the L _p decrease during the first day of salinity stress.     

Decrease in membrane hydraulic conductance of rhizodermal cells under nitrate deficit is related to acidification at the root surface

Barley seedlings (Hordeum vulgare L.) were grown on porous plates submerged in Knop medium at pH 6.0 (control) and in a similar nutrient solution where NO ₃ ^? was replaced with Cl^? (treatment); in some treatments Mes buffer (10–20 mM, pH 6.0) was added to the medium. In the absence of buffer, the pH of the medium shifted towards the alkaline region in the presence of NO ₃ ^? and to the acidic region in the presence of Cl^?, with the total shift of no more than 0.3 pH units per day. The replacement of NO ₃ ^? with Cl^? (in a buffer-free medium) decreased the hydraulic membrane conductance of rhizodermal cells (L _p) within a 4-h period; after one day L _p settled at approximately 50% of its initial value observed in untreated plants. When the removal of nitrate from the medium was accompanied by the addition of buffer, no changes in L _p were observed over a 1-day period. The perfusion of external solution (at a rate of 10 mm/s) made it possible to control pH in the proximity to root surface (pH_s). These experiments showed that L _p was independent of the surface pH in the pH_s range 7.0–5.0, whereas at pH_s = 4.5 L _p decreased within 15 min to a steady-state level of about 50% of the control value. It is concluded that the reduction of L _p under nitrate deficit was related to acidification of the medium near the root surface. The acidic pH shift could be caused by the cessation of proton/nitrate symport and by activation of the plasmalemma H⁺-pump, related to changes in the cytosolic pH-stat.     

Singlet oxygen scavenging activity of tocopherol and plastochromanol in Arabidopsis thaliana: relevance to photooxidative stress

In the present study, singlet oxygen (¹O₂) scavenging activity of tocopherol and plastochromanol was examined in tocopherol cyclase‐deficient mutant (vte1) of Arabidopsis thaliana lacking both tocopherol and plastochromanol. It is demonstrated here that suppression of tocopherol and plastochromanol synthesis in chloroplasts isolated from vte1 Arabidopsis plants enhanced ¹O₂ formation under high light illumination as monitored by electron paramagnetic resonance spin‐trapping spectroscopy. The exposure of vte1 Arabidopsis plants to high light resulted in the formation of secondary lipid peroxidation product malondialdehyde as determined by high‐pressure liquid chromatography. Furthermore, it is shown here that the imaging of ultra‐weak photon emission known to reflect oxidation of lipids was unambiguously higher in vte1 Arabidopsis plants. Our results indicate that tocopherol and plastochromanol act as efficient ¹O₂ scavengers and protect effectively lipids against photooxidative damage in Arabidopsis plants.     

Accelerated root growth induced by nitrate deficit is related to apoplast acidification

We measured the rate of growth, osmotic pressure, hydraulic conductance, longitudinal and transverse extensibility of barley (Hordeum vulgare L.) roots in Knop solution with nitrate and at substitution of NO₃⁻ with Cl⁻. During the first three days after NO₃⁻ removal, root growth acceleration was related to the increase in their longitudinal extensibility. It was shown that root exposure to buffer with pH 4.5 and also activation of H⁺ pump with naphthyl acetate imitated changes in extensibility induced by NO₃⁻ deficit. Earlier, we have demonstrated medium acidification near root surface and calculated its expected level (pH 4.5). This permits a supposition that the cause for changes in extensibility and root growth acceleration at NO₃⁻ deficit was apoplast acidification, evidently related to the ceasing of NO₃⁻ symport with H⁺ and activation of the plasmalemmal H⁺ pump. ABA did not affect root extensibility at pH 4.5; however, at pH 6.0, it was similar to the action of diethylstilbestrol, an inhibitor of H⁺ pump, and opposite to the action of NO₃⁻ deficit. Thus, the absence of ABA effects on root growth, in spite of its accumulation at NO₃⁻ deficit, could be explained by apoplast acidification as well.     

Induction of P-glycoprotein functional activity and multidrug resistance by a soluble factor(s) produced by some mammalian cells.

In the previous study we have found that Djungarian hamster fibroblasts with high levels of multidrug resistance (MDR) (colchicine-resistance index RI of 1000 to 42000) produce soluble factor(s) communicating MDR to the drug-sensitive cells of the same species by elevating the functional activity of P-glycoprotein (Pgp). Here we have shown that these cells can influence human tumor cells in the same fashion. Rat hepatoma McA RH7777 cells and their colchicine-resistant derivatives are shown to produce a factor with similar effects (induction of MDR and Pgp functional activity in the drug-sensitive cells). These effects seem to depend on the drug resistance level of the donor cells. Our results show that induction of the Pgp-mediated MDR is not species-specific and the tumor cells with intrinsic MDR (arising from the tissue with a high level of Pgp expression) can produce a factor(s) communicating this type of drug resistance to the sensitive cells.