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Similarly, if ABTS ·+ is excessive, radical (A) can also further change to quinone (B).
Excessive radical production relative to antioxidant bioavailability is fundamentally related to the likelihood of macromolecule modification and underpins past and present attempts to prevent/treat diseases using antioxidant therapy [31].
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A theoretical kinetics model was developed to determine conditions under which the spin-adduct DMPO-OH is not further oxidized by Fe3+ and excessive radicals, so that hydroxyl radicals concentration could be accurately inferred.
Normal protective mechanisms may be overwhelmed in cases of excessive free radical production; cellular damage will ensue in these situations unless additional free radical scavenging capabilities are available through dietary constituents or other exogenous sources.
Generation of excessive free radical is considered the cause of apoptosis and DNA damage [36, 37].
Asthma is a chronic inflammatory disease with excessive free radical generation in lungs and blood cells.
Sepsis and septic shock is characterized by oxidative stress that mainly promotes systemic inflammation and organ failure due to excessive free radical production and depletion of antioxidant defenses.
Excessive free radical formation has been implicated as one of the causative factors in neurotoxic damage associated with variety of metals, including methylmercury (MeHg).
Excessive free radical production has been implicated in aging related mobility reduction and various muscle diseases such as Duchenne muscular dystrophy (reviewed in [2], [48] [51]).
For example, Kumar et al. showed that administration of resveratrol in rats that received an intracerebroventricular colchicine injection, known to cause loss of cholinergic neurons and cognitive dysfunction that is associated with excessive free radical generation, had a neuroprotective role against colchicine-induced disturbances [40].
Carcinogenesis is also related to excessive free radical formation.
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