Neurological tissue damage

The modification of amino acids in proteins and peptides by oxidative processes plays a major role in the development of disease and in aging (Halliwell and Gutteridge, 1989, 1990 Kim et al., 1985 Tabor and Richardson, 1987 Stadtman, 1992). Tissue damage through free radical oxidation is known to cause various cancers, neurological degenerative conditions, pulmonary problems, inflammation, cardiovascular disease, and a host of other problems. Oxidation of protein structures can alter activity, inhibit normal protein interactions, modify amino acid side chains, cleave peptide bonds, and even cause crosslinks to form between proteins. 

Fatty acid dimers, (II), trimers, and tetramers effective as PLA2 inhibitors having antioxidant and anti-inflammatory properties were prepared by Franson (2) and used in treating nerve and tissue damage in central and peripheral neurological inflammatory conditions. 

Sanchez Mejia RO, Ona VO, Li M, Friedlander RM. Minocycline reduces traumatic brain injury-mediated caspase-1 activation, tissue damage, and neurological dysfunction. Neurosurgery 2001 48 1393-1399 discussion 1399-1401. 

Mojave rattlesnake (Crotalus scutulatus) bites deserve special consideration and caution, because neurologic signs and symptoms of envenomation may be delayed and there is often little swelling or evidence of tissue damage. The onset of muscle weakness, ptosis, and respiratory arrest may occur several hours after envenomation. Facial and laryngeal edema have also been reported. 

With modest impairment of blood flow, this mechanism allows for preservation of oxidative metabolism without alteration in electrical function. However, when CPP and therefore CBF are sufficiently low, OEF reaches a maximum and cannot increase further. Brain tissue ceases to function electrically, resulting in a neurologic deficit. Microvascular collapse occurs, and CBV falls. If the oxygen supply falls low enough, the tissue dies. Of critical clinical importance is the observation that the amount of time it takes for tissue to suffer irreversible damage is inversely related to the severity of the ischemic insult. Tissue that is completely deprived of blood will die within a few minutes, but less severely hypoperfused tissue may survive for many hours, and may be saved by timely thrombolysis that restores perfusion, or perhaps by another therapeutic intervention. 

Zivin JA, Fisher M, DeGirolami U, Hemenway CC, Stashak JA. Tissue plasminogen activator reduces neurological damage after cerebral embolism. Science. 1985 230 1289-1292. 

Zivin JA, Lyden PD, DeGirolami U, Kochhar A, Mazzarella V, Hemenway CC, Johnston P. Tissue plasminogen activator. Reduction of neurologic damage after experimental embolic stroke. Arch Neurol. 1988 45 387-391. 

An anti-intracellular adhesion molecule-1 (anti-ICAM-1) antibody reduced neurological damage in a rabbit embolic model of stroke followed by thrombolysis with tissue-type plasminogen activator (tPA). When thrombolysis was delayed for 3 h following embolism, neither tPA nor the tPA/ICAM combination reduced neurological damage. 

Of the 16 POPs listed in the 1998 Aarhus Protocol [27], 11 are organochloride pesticides, which have now been banned in several countries. Most concerns regarding these products relate to their toxicity, with health effects to humans ranging from lung damage and neurological problems to death. Many organochloride pesticides are lipophilic, and they accumulate in the adipose tissues. 

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