Oxidative stress is suspected to be important in neurodegenerative diseases including Lou Gehrigs disease (aka MND or ALS), Parkinsons disease, Alzheimers disease, Huntingtons disease, depression, and multiple sclerosis. It is also indicated in Neurodevelopmental conditions such as Autism Spectrum Disorder. Indirect evidence via monitoring biomarkers such as reactive oxygen species, and reactive nitrogen species production indicates oxidative damage may be involved in the pathogenesis of these diseases, while cumulative oxidative stress with disrupted mitochondrial respiration and mitochondrial damage are related to Alzheimers disease, Parkinsons disease, and other neurodegenerative diseases.
Oxidative stress is thought to be linked to certain cardiovascular disease, since oxidation of LDL in the vascular endothelium is a precursor to plaque formation.  Oxidative stress also plays a role in the ischemic cascade due to oxygen reperfusion injury following hypoxia.  This cascade includes both strokes and heart attacks. Oxidative stress has also been implicated in chronic fatigue syndrome (ME/CFS). Oxidative stress also contributes to tissue injury following irradiation and hyperoxia, as well as in diabetes. In hematological cancers, such as leukemia, the impact of oxidative stress can be bilateral. Reactive oxygen species can disrupt the function of immune cells, promoting immune evasion of leukemic cells. On the other hand, high levels of oxidative stress can also be selectively toxic to cancer cells.
Oxidative stress is likely to be involved in age-related development of cancer.  The reactive species produced in oxidative stress can cause direct damage to the DNA and are therefore mutagenic, and it may also suppress apoptosis and promote proliferation, invasiveness and metastasis.  Infection by Helicobacter pylori which increases the production of reactive oxygen and nitrogen species in human stomach is also thought to be important in the development of gastric cancer.
Oxidative stress can cause DNA damage in neurons.  In neuronal progenitor cells, DNA damage is associated with increased secretion of amyloid beta proteins Aβ40 and Aβ42. This association supports the existence of a causal relationship between oxidative DNA damage and Aβ accumulation and suggests that oxidative DNA damage may contribute to Alzheimer's disease (AD) pathology.  AD is associated with an accumulation of DNA damage (double-strand breaks) in vulnerable neuronal and glial cell populations from early stages onward, and DNA double-strand breaks are increased in the hippocampus of AD brains compared to non-AD control brains.