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Review
. 2021 Jun 2;22(11):6014.
doi: 10.3390/ijms22116014.

Bladder Hyperactivity Induced by Oxidative Stress and Bladder Ischemia: A Review of Treatment Strategies with Antioxidants

Yi-Hsuan Wu  1   2   3 , Kuang-Shun Chueh  1   2   4 , Shu-Mien Chuang  2 , Cheng-Yu Long  5   6 , Jian-He Lu  7 , Yung-Shun Juan  1   2   4   6
Affiliations
Review

Bladder Hyperactivity Induced by Oxidative Stress and Bladder Ischemia: A Review of Treatment Strategies with Antioxidants

Yi-Hsuan Wu et al. Int J Mol Sci. .

Abstract

Overactive bladder (OAB) syndrome, including frequency, urgency, nocturia and urgency incontinence, has a significantly negative impact on the quality-of-life scale (QoL) and can cause sufferer withdrawal from social activities. The occurrence of OAB can result from an imbalance between the production of pro-oxidants, such as free radicals and reactive species, and their elimination through protective mechanisms of antioxidant-induced oxidative stress. Several animal models, such as bladder ischemia/reperfusion (I/R), partial bladder outlet obstruction (PBOO) and ovarian hormone deficiency (OHD), have suggested that cyclic I/R during the micturition cycle induces oxidative stress, leading to bladder denervation, bladder afferent pathway sensitization and overexpression of bladder-damaging molecules, and finally resulting in bladder hyperactivity. Based on the results of previous animal experiments, the present review specifically focuses on four issues: (1) oxidative stress and antioxidant defense system; (2) oxidative stress in OAB and biomarkers of OAB; (3) OAB animal model; (4) potential nature/plant antioxidant treatment strategies for urinary dysfunction with OAB. Moreover, we organized the relationships between urinary dysfunction and oxidative stress biomarkers in urine, blood and bladder tissue. Reviewed information also revealed the summary of research findings for the effects of various antioxidants for treatment strategies for OAB.

Keywords: antioxidants; bladder dysfunction; overactive bladder; oxidative stress.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Disorders associated with oxidative stress and overactive bladder (OAB), including bladder I/R, PBOO, metabolic syndrome, and ovary hormone depletion (OHD). OAB syndrome includes frequency, urgency, nocturia and urgency incontinence. The occurrence of OAB may result from an imbalance between the production of pro-oxidants and their elimination through antioxidants. Several animal models mimic the physiological condition to induce OAB, such as bladder ischemia/reperfusion (I/R), partial bladder outlet obstruction (PBOO), metabolic syndrome and ovarian hormone deficiency (OHD). Oxidative stress is regulated by the balance between pro-oxidative and antioxidative factors. Oxidative stress increased the levels of cellular reactive oxygen species (ROS), reactive nitrogen species (RNS) and free radicals. The antioxidant defense system participates in scavengers of free radicals to decrease excessive ROS and protect against oxidative-stress-induced bladder dysfunction. Redox signaling is essential for the maintenance of homeostasis between oxidants (ROS generation) and antioxidants (ROS elimination). ROS are derived from nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX), xanthine oxidase, nitric oxide synthase (NOS) and cyclooxygenases’ mitochondrial respiratory chain. Cellular ROS levels are regulated by an enzymatic antioxidant system. The defense systems include enzymes such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px). However, excessive production of ROS/RNS can cause oxidative stress, which results in DNA damage, protein adducts, lipid peroxidation, mitochondrial dysfunction and immune cell infiltration in bladder tissue leading to bladder denervation and increasing fibrosis and apoptosis, resulting in bladder hyperactivity.
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