Oxidative stress and its possible relation to lower urinary tract functional pathology

Abstract

Oxidative stress is considered to reflect an imbalance between the systemic manifestation of reactive oxygen and nitrogen species (RONS) and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. RONS are not only harmful agents that cause oxidative damage in pathologies; they also have important roles as regulatory agents in a range of biological phenomena. They are normally generated as by-products of oxygen metabolism; however, environmental stressors (i.e., ultraviolet radiation, ionizing radiations, pollutants, heavy metal, and xenobiotics) contribute to greatly increase RONS production. Several antioxidants have been exploited in recent years for their actual or supposed beneficial effect against oxidative stress, but to date, none has been approved for any indication because they have not met the criteria of efficacy for drug approval. The present review discusses the concept of oxidative stress, how to measure it, how to prevent it, and its occurrence in different organ systems with special reference to the lower urinary tract.

Advances in the mechanism of high copper diets in restraining pigs growth

“…Damage to the liver and kidneys may cause dysfunction of metabolic systems and limit the involvement of these organs in regulating the growth axis. These series of changes may restrain the growth of pigs (Kumar et al, 2016a) [Colour figure can be viewed at wileyonlinelibrary.com] haematuria and proteinuria, which may cause urinary tract infections and seriously affect the growth performance of pigs (Andersson, 2018;Thit, Selck, & Bjerregaard, 2015). During kidney injury, there is a simultaneous cell adhesion molecules, cytokine-chemokine expression, leucocyte trafficking, apoptosis dysregulation and oxidative stress in distant organs such as the lung (Mehta, Pascual, Gruta, Zhuang, & Chertow, 2002), liver (Sural et al, 2000), heart (Blake et al, 1996), intestinal tract ( Di Giancamillo et al, 2018Slack & Wendon, 2009) and brain (Burn & Bates, 1998) and haematological system may occur.…”

Gintonin-Enriched Fraction Suppresses Heat Stress-Induced Inflammation through LPA Receptor

“…High temperature environments such as those due to global warming or hot summer seasons causes heat stress, which generates reactive oxygen species (ROS) and causes oxidative stress [1]. Oxidative stress is caused by an imbalance between the production of reactive oxygen species in the body and the ability of the biological system to remove them [2]. The redox imbalance of cells can cause toxic effects through the production of peroxides and free radicals that damage all components of the cell, including proteins, lipids, and DNA [3].…”

Relationship between oxidative stress and lower urinary tract symptoms: results from a community health survey in Japan

“…A link between bladder ischaemia and oxidative stress has been suggested to be related to LUTS in animal models ; however, few studies have addressed the direct association between LUTS and oxidative stress in humans . 8‐Hydroxy‐2′‐deoxyguanosine (8‐OHdG) is one of the most common markers of oxidative DNA damage . Advanced glycation end products (AGEs), a group of harmful compounds, modified proteins, and/or lipids with damaging potential, are among the surrogate markers of oxidative stress .…”

“…AGE levels, measured by skin autofluorescence of the forearm, are elevated in patients with diabetes, renal failure, vascular complications and coronary heart disease . As skin AGEs are potentially associated with vascular damage, including in the urinary bladder, the increased production and augmentation of oxidative stress may contribute to the development of LUTS . Little is known, however, about the effect of oxidative stress on the aetiology of LUTS .…”

“…As skin AGEs are potentially associated with vascular damage, including in the urinary bladder, the increased production and augmentation of oxidative stress may contribute to the development of LUTS . Little is known, however, about the effect of oxidative stress on the aetiology of LUTS . We aimed to investigate the relationships among LUTS, 8‐OHdG levels and AGE levels in a community‐dwelling population.…”