Influence of oxidative stress on inducing micturition dysfunction following chronic infravesical obstruction and the protective role of an antioxidant diet - association of in vivo and in vitro studies in rats

Abstract

ARTIcLE INFO _________________________________________________________ ___________________Objective: This study was developed to determine whether the generation of free radicals, induced by ischemia followed by reperfusion in a model of chronic intravesical obstruction in rats, would lead to damage in the detrusor. It also investigates the possible protective action of the flavonoid galangin on the tissue lesion induced by lipid peroxidation. Materials and Methods: Twenty-one male rats were divided into three groups of seven animals each. Group A was subjected to a sham procedure; group B to partial obstruction of the bladder neck; and group C to partial obstruction of the bladder neck, but also received a diet rich in the flavonoid galangin. All the animals were subjected to urodynamic evaluation and then sacrificed. The bladders were sent for enzymatic tests. Results:The urodynamic showed that group B developed significantly greater numbers of involuntary contractions of the detrusor, greater post-micturition residue and lower compliance. The group A presented TEAC levels greater than to the group B. Comparative analysis of group A, B and C demonstrated significantly greater malondialdehyde levels in group B in relation to groups A and C. The group B presented smaller contraction amplitudes than did groups A and C, in electrically stimulated contractions. Conclusions: That oxidative stress is implicated in the damage to the detrusor musculature following a period of chronic intravesical obstruction. We show, for the first time, that administration of an antioxidant prior to and following the start of chronic obstruction makes it possible to avoid the cellular lesions that cause detrusor dysfunction.

The NLRP3 Inflammasome Mediates Inflammation Produced by Bladder Outlet Obstruction

“…Since we did not perform serial measurements to document the temporal appearance of each phase, it is not possible to completely rule out this possibility. However, as stated above we are working with a time frame that would be considered early in rat BOO, 16–22 making it unlikely these bladders have decompensated. The more likely explanation for the decreased void volumes is that the procedure we used to create obstruction produces a severe enough increase in resistance that the bladder cannot generate sufficient force to overcome it, even in the early phase.…”

Oxidative stress and antioxidant defence markers in muscle tissue of rainbow trout (Oncorhynchus mykiss) after vaccination against Yersinia ruckeri

“…This occurs because the polyunsaturated fatty acids of cell membranes are degraded by this process, with consequent rupture of membrane integrity. Membrane peroxidation may lead to changes in membrane fluidity and permeability, and may also increase protein degradation and rates of cell lysis (2,11). Lipid peroxidation has been implicated in the aetiology of damage to subcellular membranes by inactivating cell constituents through oxidation or inducing oxidative stress by undergoing radical chain reaction (1).…”

The preventive effect of a free radical scavenger on oxidative stress after the relief of partial bladder outlet obstruction in a rat model

“…Chronic I/R injury induced NVCs in the cystometrogram in our study. Oxidative stress results in the generation of free radicals and oxidative damage [ 17 ]. Chronic oxidative stress may damage intrinsic nerves, resulting in partial denervation of smooth muscle.…”

“…Denervation and nerve degeneration in sensory pathways during chronic I/R injury also cause an increase in the nerve growth factor level that may induce bladder hypersensitivity [ 19 ]. Additionally, chronic oxidative stress leads to the accumulation of calcium in the intracellular medium and the formation of metabolic end products that damage the detrusor musculature [ 17 ]. The resulting neurogenic and myogenic damage may cause detrusor overactivity but impaired contractility, resulting in NVCs in the cystometrogram.…”