Results: 4

1.
2

2. From: ANTIOXIDANT THERAPIES FOR TRAUMATIC BRAIN INJURY.

Chemical reactions of 4-HNE with amino acids that lead to impairment of protein structure and function.

Edward D. Hall, et al. Neurotherapeutics. ;7(1):51.
2.
3

3. From: ANTIOXIDANT THERAPIES FOR TRAUMATIC BRAIN INJURY.

Chemical structures of lipid peroxyl radical scavenging and nitroxide-containing antioxidants shown to be neuroprotective in TBI models.

Edward D. Hall, et al. Neurotherapeutics. ;7(1):51.
3.
1

1. From: ANTIOXIDANT THERAPIES FOR TRAUMATIC BRAIN INJURY.

Chemistry involved in the initiation, propagation and termination reactions of arachidonic acid during lipid peroxidation with the resulting formation of the aldehydic end-product 4-hydroxynonenal (4-HNE).

Edward D. Hall, et al. Neurotherapeutics. ;7(1):51.
4.
4

4. From: ANTIOXIDANT THERAPIES FOR TRAUMATIC BRAIN INJURY.

Rationale for combination antioxidant therapy for TBI. Injury triggers an increase in cytoplasmic Ca++ via voltage dependent and glutamate receptor-operated channels. The increase in intracellular Ca++ initiates activation of cytoplasmic calpain. Mitochondrial Ca++ uptake (buffering) stresses the mitochondria and contributes to mitochondrial dysfunction Specifically, Ca++ uptake by the mitochondria leads O2•- leakage from the electron transport chain and activation of Ca++-activated mitochondrial nitric oxide synthase (NOS). The O2•- and NO● combine to form the potent reactive nitrogen species PN which is able to which in turn gives rise to the highly reactive nitrogen dioxide (•NO2), hydroxyl (•OH) and carbonate (•CO3) radicals which cause oxidative damage to the mitochondria as well as other cellular structures due to PN’s large diffusion radius. When this becomes severe, there is a decrease in the mitochondrial ATP production and membrane potential (ΔΨ). This leads to catastrophic mitochondrial failure (mitochondrial permeability transition, MPT) and the dumping of mitochondrial Ca++ into the cytoplasm where it exacerbates cytoplasmic calpain activation and proteolysis of a cytoskeletal proteins and other substrates. The combination of the antioxidant tempol which catalytically reacts with PN-derived radicals with a chain-breaking LP inhibitor such as U-83836E or a carbonyl (CHO) scavenging compound should produce a better neuroprotective effect than any of these compounds alone.

Edward D. Hall, et al. Neurotherapeutics. ;7(1):51.

Supplemental Content

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Write to the Help Desk