Oxidative Damage

Overview

Oxidative damage is the harm caused to cellular components when reactive oxygen species (ROS) and other free radicals exceed the body's capacity to neutralize them. ROS are produced naturally as by-products of normal metabolic processes, but when their levels become excessive a state of oxidative stress develops, in which these reactive molecules attack and impair essential biomolecules including DNA, proteins, and lipids. This molecular damage is implicated in the pathogenesis of numerous conditions, such as cancer, diabetes, cardiovascular disease, inflammatory disorders, neurodegenerative diseases, and the broader process of biological aging. The body counters ROS through antioxidant defenses, including endogenous enzymes and dietary antioxidants and phytochemicals that scavenge free radicals and help restore redox balance. In line with its focus on antioxidant activity, this journal publishes research examining oxidative damage and its mitigation, including the effects of ozone and oxygen molecules on testicular and sperm mitochondria, the radical-scavenging and antioxidative activity of specific compounds in cell-free and cardiomyoblast systems, antioxidant phytochemicals as potential treatments for age-related macular degeneration, the antioxidant and hepatoprotective activity of tea polysaccharides, oxidative telomere attrition in relation to nutritional antioxidants and aging, the redox potential of phytochemicals and their impact on DNA, and protective effects against chemically induced liver oxidative stress.

Research published in this journal

12 peer-reviewed articles, ranked by relevance. Each links to its DOI.

How this research is being cited

The 12 articles above have been cited 85 times in the scholarly literature. Citation data via OpenAlex and Crossref, updated Nov 2026.

• Vonoprazan attenuates cyclophosphamide-induced ovarian injury in rats via modulation of TLR4/NF-κB and AMPK/SIRT1/Nrf2/HO-1 signaling
  2027 · Tissue and Cell
• Buspirone combats cyclophosphamide-provoked hepatotoxicity in rats via activation of AMPK/Nrf2/HO-1 and suppression of NF-κB p65 /NLRP3 inflammasome pathways
  2026 · Naunyn-Schmiedeberg's Archives of Pharmacology
• Increasing viability of pathological liver grafts from brain dead donors via intestinal parasympathetic nerve stimulation, or exogenous serotonin
  2026 · Scientific Reports
• Astragalus polysaccharides ameliorate ulcerative colitis by targeting the HMGB1/TLR4 signaling axis to inhibit neutrophil extracellular trap formation
  2026 · Cellular Immunology
• Melatonin attenuates diquat-induced acute liver injury by modulating Nrf2-Associated antioxidant signaling and ferroptosis-related processes
  2026 · Science Progress
• Increasing viability of pathological liver grafts from brain dead donors via intestinal parasympathetic nerve stimulation, or exogenous serotonin
  2026 · Scientific Reports
• Advances in chrysin research for cardiovascular disorders: mechanistic insights and therapeutic prospects
  2026 · Molecular Biology Reports
• Sacubitril/valsartan attenuates renal injury caused by cecal ligation and puncture via TLR4/NFκB/NLRP3 inhibition and reduced oxidative stress and apoptosis in rats
  2026 · Scientific Reports

A sample of recent works citing this journal's research on Oxidative Damage, linking to each citing work.

This page summarises published research for orientation; it is not medical or professional advice.

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