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The 21-aminosteroid ("lazaroid") U-74389G (U74), an inhibitor of lipid peroxidation (LP), was used to protect mitochondrial function following TBI in young adult male rats. The animals received a severe (2.2 mm) controlled cortical impact-TBI.

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Free radicals and other so-called 'reactive species' are constantly produced in the brain in vivo. Some arise by 'accidents of chemistry', an example of which may be the leakage of electrons from the mitochondrial electron transport chain to generate superoxide radical (O2*-). Others are generated for useful purposes, such as the role of nitric oxide in neurotransmission and the production of O2*- by activated microglia.

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Effects of dietary restriction and antioxidants on presbyacusis.

Laryngoscope

May 2000

Department of Otolaryngology-Head and Neck Surgery, Henry Ford Health System, West Bloomfield, Michigan 48323, USA.

Objectives/hypothesis: The premise of this study is that the membrane hypothesis of aging, also known as the mitochondrial clock theory of aging, is the basis for presbyacusis. Furthermore, it is proposed that treatment with antioxidants or dietary restriction can attenuate age-related hearing loss. Many studies have demonstrated a reduction in blood flow to specific tissues, including the cochlea, with aging.

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Reactive oxygen metabolites, antioxidants and head and neck cancer.

Head Neck

August 1999

Department of Otolaryngology-Head and Neck Surgery, Henry Ford Hospital, 6777 W. Maple Road, W. Bloomfield, MI 48323, USA.

This manuscript will review the probable role of reactive oxygen metabolites (ROM) in the etiopathogenesis of head and neck cancer (HNC). Cancer is a heterogeneous disorder with multiple etiologies including somatic and germ-line mutations, cellular homeostatic disturbances, and environmental triggers. Certain etiologies are characteristic of HNC and include infectious agents such as the Epstein-Barr virus, the use of tobacco, and consumption of alcohol.

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Chronic exposure to low levels of lead results in sustained hypertension (HTN) in humans and experimental animals. The mechanism of lead-induced HTN remains unclear. We investigated the possible role of reactive oxygen species (ROS) and their impact on nitric oxide (NO) metabolism in lead-induced HTN.

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