Free radicals and related reactive species as mediators of tissue injury and disease: implications for Health

Abstract

A radical is any molecule that contains one or more unpaired electrons. Radicals are normal products of many metabolic pathways. Some exist in a controlled (caged) form as they perform essential functions. Others exist in a free form and interact with various tissue components. Such interactions can cause both acute and chronic dysfunction, but can also provide essential control of redox regulated signaling pathways. The potential roles of endogenous or xenobiotic-derived free radicals in several human pathologies have stimulated extensive research linking the toxicity of numerous xenobiotics and disease processes to a free radical mechanism. In recent years, improvements in analytical methodologies, as well as the realization that subtle effects induced by free radicals and oxidants are important in modulating cellular signaling, have greatly improved our understanding of the roles of these reactive species in toxic mechanisms and disease processes. However, because free radical-mediated changes are pervasive, and a consequence as well as a cause of injury, whether such species are a major cause of tissue injury and human disease remains unclear. This concern is supported by the fact that the bulk of antioxidant defenses are enzymatic and the findings of numerous studies showing that exogenously administered small molecule antioxidants are unable to affect the course of most toxicities and diseases purported to have a free radical mechanism. This review discusses cellular sources of various radical species and their reactions with vital cellular constituents, and provides examples of selected disease processes that may have a free radical component.

Antioxidant and anti-inflammatory properties of selected polyherbal preparations: Oroki herbal, Swedish bitters and Yoyo bitters

“…These chemical radicals are important mediators in provoking or sustaining inflammatory processes, and consequently, their neutralization by phyto-antioxidants may attenuate inflammatory response [15].…”

Nephroprotective Effect of Low Viscosity Sodium Alginate on Lead Acetate-Induced Nephrotoxicity in Rats

“…All of which may interact with proteins, DNA, and RNA in the cell causing renal tissue damage. 28 Here, LvSA has been shown to reduce LPO production and considerable effect in augment LAinduced nephrotoxicity. The findings of the histological study support the above mentioned results, whether for the effect of LA or the preventive effects of the LvSA.…”

The protective roles of zinc and estradiol in renal ischemia/reperfusion injury in ovariectomized rats

“…One of the key events in the pathology of renal damage after IRI is overproduction of ROS and/or decrease the antioxidant capacity (9). Free radical production promotes kidney injury via lipids peroxidation and proteins and DNA oxidative damage (10). The kidney injury may also increase by inflammatory cascade via releasing of the ROS, cytokines, and leukocytes activation (11,12).…”