Free radical processes and loss of seed viability during desiccation in the recalcitrant species Quercus robur L.

1992 ◽  
Vol 122 (2) ◽  
pp. 273-279 ◽  
Author(s):  
GEORGE A. F. HENDRY ◽  
WILLIAM E. FINCH-SAVAGE ◽  
P. CHRISTOPHER THORPE ◽  
NEIL M. ATHERTON ◽  
SARAH M. BUCKLAND ◽  
...  
1993 ◽  
Vol 3 (3) ◽  
pp. 141-153 ◽  
Author(s):  
George A. F. Hendry

AbstractThe origin and significance of free radicals is described in the broad setting of animal and plant biology and in the specific context of seeds and seed viability. Evidence is given that free radicals play a central if not causal role in promoting molecular damage under the widest range of environmental stresses and induced ageing in mature plant tissuesIn ungerminated seeds, the evidence is less certain. The reason, we argue, is that many attempts to measure free radical processes in seeds are set not against gradients of damage or ageing (as they are in most other biological tissues) but against one of only two options, either seed germinability or mortality. Because free radical reactions differ quantitatively and qualitatively in living and dead tissues attempts to correlate radicalmediated damage with the viability of a population of seeds may be unreliable particularly when measurements are made at uncertain intervals after death. Despite this, the evidence that seeds, uniquely, are exempt from the ravages of oxygen assault is weak. Instead it ismore probable that oxygen plays a central role in seed mortality and may have significance in the evolution of seed persistence.


Author(s):  
A. G. Zhukova ◽  
L. G. Gorokhova ◽  
A. S. Kazitskaya ◽  
T. K. Yadykina ◽  
N. N. Mikhailova ◽  
...  

Introduction. Fluorine compounds in small doses, but with prolonged exposure, cause various disorders in organs at the cellular and molecular levels. Activation of free-radical processes plays an important role in the damaging eff ect of fl uorides. Th erefore, one of the most eff ective ways to limit fl uorine-induced damage is to directly aff ect free-radical processes using herbal preparations with antioxidant properties.The aim of the study is to study the eff ect of a dihydroquercetin-based drug on the activity of free radical processes in brain tissue under subchronic exposure to sodium fl uoride (NaF).Materials and methods. Th e work was performed on white male laboratory rats weighing 200-250 g. Th e rats were divided into 3 groups: 1 — control; 2 — rats with chronic exposure to sodium fl uoride (NaF) for 9 weeks; 3 — rats receiving a NAF solution with simultaneous administration of a complex drug based on dihydroquercetin at a dose of 3 mg/kg in 1% starch gel for 3, 6 and 9 weeks. The activity of free radical oxidation and antioxidant defense enzymes — superoxide dismutase (SOD) and catalase-was determined in the cerebral cortex. Th e level of expression of hypoxia-induced transcription factor HIF — 1A and inducible forms of proteins HSP72 and HSP32 were determined in the cytosolic fraction of brain tissue.Results. In the early stages of subchronic fl uoride exposure (1-3 weeks), the expression of protective proteins HIF-1α, HSP72, HSP32 and catalase was shown in the rat cortex, as a result of which the activity of free-radical processes was maintained at the control level. An increase in the timing of fl uoride intake to 9 weeks led to a decrease in antioxidant protection and signifi cant activation of free radical oxidation in brain tissue. Daily administration of a complex drug with dihydroquercetin for 3, 6 and 9 weeks to rats with subchronic fl uoride exposure led to a decrease in the severity of pro- and antioxidant balance disorders in the cerebral cortex. At the same time, the greatest protective eff ect of dihydroquercetin with fl uoride exposure was manifested by the 9th week of its administration.Conclusions. When subchronic intake of fl uorides in the body, the drug based on dihydroquercetin has a neuroprotective eff ect, which is manifested by an increase in the activity of antioxidant enzymes of fr ee radical oxidation and catalase and the resistance of the cortex to induced fr ee radical oxidation.


2007 ◽  
Vol 1 (3) ◽  
pp. 245-248
Author(s):  
D. A. Miskevich ◽  
N. E. Petushok ◽  
V. V. Lelevich ◽  
S. V. Lelevich ◽  
A. N. Borodinsky

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