Oxidative stress is a phenomenon caused by an imbalance between the production and accumulation of reactive oxygen species (ROS) in cells and tissues and the ability of a biological system to detoxify these reactive products. ROS can play, and they do it, several physiological roles (i.e., cell signaling), and they are normally generated as by-products of oxygen metabolism; despite this, environmental stressors (i.e., UV, ionizing radiations, pollutants, and heavy metals) and xenobiotics (i.e., antiblastic drugs) contribute to significantly increasing ROS production, therefore causing the imbalance that leads to cell and tissue damage (oxidative stress). If not strictly controlled, oxidative stress can induce several chronic and degenerative diseases, speeding up the body’s ageing process and causing acute pathologies (i.e., trauma and stroke). Most in vivo and in vitro studies have shown that oxidative stress and free radicals are confirmed to be responsible for several pathological conditions affecting different tissues and systems, thus being one of the most essential and pervasive harms to human health.

Cancer onset in humans is a complex process requiring cellular and molecular alterations mediated by endogenous and exogenous triggers. It is already well known that oxidative DNA damage is one of those stimuli responsible for cancer development. Cancer can be driven and promoted by chromosomal abnormalities and oncogene activation determined by oxidative stress. Hydrolyzed DNA bases are typical by-products of DNA oxidation and are considered one of the most relevant events in chemical carcinogenesis. Oxidative stress resulting from lifestyle reasons can also play a crucial role in cancer development, as suggested by the strong correlation between dietary fat consumption (a factor that exposes the organism to a greater risk of lipid peroxidation) and death rates from different types of cancer.

Cardiovascular diseases (CVDs) are clinical entities with a multifactorial etiology, generally associated with many risk factors. During the last few years, research data pointed out that oxidative stress should be considered a primary or a secondary cause for many CVDs. Oxidative stress acts mainly as a trigger of atherosclerosis. It is well known that atheromatous plaque formation results from early endothelial inflammation, leading ROS generation by macrophages recruited in situ. Circulating LDL is then oxidized by reactive oxygen species, thus leading to foam cell formation and lipid accumulation. The result of these events is the formation of an atherosclerotic plaque. Both in vivo and ex vivo studies provided evidence supporting the role of oxidative stress in atherosclerosis, ischemia, hypertension, cardiomyopathy, cardiac hypertrophy, and congestive heart failure.

Oxidative stress has been linked to several neurological diseases (i.e., Parkinson’s disease, Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), multiple sclerosis, depression, and memory loss). In AD, several experimental and clinical research showed that oxidative damage plays a pivotal role in neuron loss and progression to dementia. β-amyloid, a toxic peptide often found in AD patients’ brains, is produced by free radical action. It is known to be at least in part responsible for neurodegeneration observed during AD onset and progression.

Lung diseases such as asthma and chronic obstructive pulmonary disease (COPD), determined by systemic and local chronic inflammation, are linked to oxidative stress. Oxidants are known to enhance inflammation by activating different kinases involving pathways and transcription factors.

Rheumatoid arthritis is a chronic inflammatory disorder affecting the joints and surrounding tissues, characterized by macrophages and activated T-cell infiltration. Free radicals at the site of inflammation play a relevant role in the initiation and progression of this syndrome, as demonstrated by the increased isoprostane and prostaglandin levels in the synovial fluid of affected patients.

Oxidative stress also involves glomerulo- and tubule-interstitial nephritis, renal failure, proteinuria, and uremia. The kidneys are negatively affected by oxidative stress mainly because ROS production recruits inflammatory cells and proinflammatory cytokine production, leading to an initial inflammatory stage. Heavy (Cd, Hg, Pb, and As) and transition metals (Fe, Cu, Co, and Cr), acting as powerful oxidative stress inducers, are responsible for various forms of nephropathy, as well as for some types of cancers.

Oxidative stress could be responsible for delayed sexual maturation and puberty onset. This seems to be true when children in prepubertal age are exposed to Cd, a well-known responsible for an increase in free radicals and oxidative stress, as well as when pregnant women are exposed to the same metallic element.

As a dictionary meaning, ageing is the state of being old and is used to describe a particular part of life. Ageing should be evaluated in terms of biological, psychological, and social ageing as well as chronological ageing. While the primary measure of chronological ageing is the calendar age of the person, the primary criterion for biological ageing is the cardiovascular age of the person. Significant indicators of cardiovascular ageing at the molecular level are cellular senescence, genomic instability, epigenetic changes, chromatin modification and mitochondrial oxidative stress.

Treating diseases and clinical conditions based on oxidative stress mainly includes treatments that support the regeneration of damaged tissues and organs and the recovery of body functions. Ageing, various diseases, accidents or congenital abnormalities can cause damage to the body. In such cases, regenerative medicine recommends alternative treatments to regenerate or repair the damaged tissue or organ. Among these treatment options, PRP and stem cell as innovative products are some of the methods that can be used, and ensuring healthy ageing is among the main targets. Research for the discovery of effective molecules associated with healthy ageing and delaying ageing and the treatment of oxidative stress-related clinical conditions, and investigating the pharmacological effects of possible molecules are among the main working areas of our laboratory. Additionally, research on wound healing, epilepsy, neurodegenerative diseases including Alzheimer’s and Parkinson diseases, studies on circadian rhythm, clinical pharmacology, and toxicology is ongoing in our laboratory.