The Biochemistry of Disease: Free Radical Mechanisms in Tissue Injury . T. F. Slater. Pion, London, 1972. xii, 284 pp., illus. £4.80. Pion Advanced Biochemistry Series, 1.

Science ◽  
1972 ◽  
Vol 177 (4055) ◽  
pp. 1184-1185
Author(s):  
Edward A. Smuckler
Keyword(s):  
Free Radical ◽  
Tissue Injury ◽  
Disease Free

Further studies on free-radical pathology in the major central nervous system disorders: effect of very high doses of methylprednisolone on the functional outcome, morphology, and chemistry of experimental spinal cord impact injury

1982 ◽  
Vol 60 (11) ◽  
pp. 1415-1424 ◽  
Author(s):  
H. B. Demopoulos ◽  
E. S. Flamm ◽  
M. L. Seligman ◽  
D. D. Pietronigro ◽  
J. Tomasula ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Free Radical ◽  
Tissue Injury ◽  
Functional Restoration ◽  
Radical Reactions ◽  
Free Radical Reactions ◽  
Cord Injury

The hypothesis that pathologic free-radical reactions are initiated and catalyzed in the major central nervous system (CNS) disorders has been further supported by the current acute spinal cord injury work that has demonstrated the appearance of specific, cholesterol free-radical oxidation products. The significance of these products is suggested by the fact that: (i) they increase with time after injury; (ii) their production is curtailed with a steroidal antioxidant; (iii) high antioxidant doses of the steroidal antioxidant which curtail the development of free-radical product prevent tissue degeneration and permit functional restoration. The role of pathologic free-radical reactions is also inferred from the loss of ascorbic acid, a principal CNS antioxidant, and of extractable cholesterol. These losses are also prevented by the steroidal antioxidant. This model system is among others in the CNS which offer distinctive opportunities to study, in vivo, the onset and progression of membrane damaging free-radical reactions within well-defined parameters of time, extent of tissue injury, correlation with changes in membrane enzymes, and correlation with readily measurable in vivo functions.

Free Radical Mechanisms in Tissue Injury

1988 ◽  
pp. 209-218 ◽  
Author(s):  
T. F. Slater
Keyword(s):  
Free Radical ◽  
Tissue Injury

scholarly journals Protective role of ceftriaxone plus sulbactam with VRP1034 on oxidative stress, hematological and enzymatic parameters in cadmium toxicity induced rat model

2012 ◽  
Vol 5 (4) ◽  
pp. 192-200 ◽  
Author(s):  
Vivek Kumar Dwivedi ◽  
Anuj Bhatanagar ◽  
Manu Chaudhary
Keyword(s):  
Free Radical ◽  
Tissue Injury ◽  
Cadmium Toxicity ◽  
Treated Group ◽  
Protective Role ◽  
Enzymatic Activities ◽  
Exposed Group ◽  
Male Rats ◽  
Control Group

ABSTRACT We investigated the protective role of ceftriaxone plus sulbactam with VRP1034 (Elores) on hematological, lipid peroxidation, antioxidant enzymatic activities and Cd levels in the blood and tissues of cadmium exposed rats. Twenty-four male rats were divided into three groups of eight rats each. The control group received distilled water whereas group II received CdCl2 (1.5 mg/4 ml/body weight) through gastric gavage for 21 days. Group III received CdCl2 and was treated with ceftriaxone plus sulbactam with VRP1034 for 21 days. The hematological, biochemical, lipid per-oxidation levels and enzymatic parameters were measured in plasma and tissues (brain, liver and kidney) of all groups. The Cd, Zn and Fe levels were measured in blood and tissues of all groups. Our findings showed significantly decreased cadmium (p<0.001), malonaldialdehyde (p<0.001) and myloperoxidase (MPO) levels along with significantly increased hemoglobin (p<0.01), RBC (p<0.05), hematocrit (p<0.05) levels and all antioxidant enzymatic activities (SOD, CAT, GR, GPx) in plasma and tissues of ceftriaxone plus sulbactam with VRP1034 treated group as compared to cadmium exposed group. Delta aminolevulinate dehydratase (δ-ALAD) activity was significantly (p<0.001) increased in the blood of ceftriaxone plus sulbactam with VRP1034 treated group as compared with cadmium exposed group. The levels of hepatic and renal parameters were significantly (p<0.001) decreased in ceftriaxone plus sulbactam with VRP1034 treated group as compared to cadmium exposed group. These findings indicate that ceftriaxone plus sulbactam with VRP1034 acts as a potent free radical scavenger and exhibits metal chelating properties that reduce free radical mediated tissue injury and prevent dysfunction of hepatic and renal organs during metal intoxication.

Protection from hyperbaric oxidant stress by administration of buthionine sulfoximine

1991 ◽  
Vol 71 (1) ◽  
pp. 352-358 ◽  
Author(s):  
K. H. Komadina ◽  
C. A. Duncan ◽  
C. L. Bryan ◽  
S. G. Jenkinson
Keyword(s):  
Free Radical ◽  
Direct Effect ◽  
Tissue Injury ◽  
Oxidant Stress ◽  
Buthionine Sulfoximine ◽  
Antioxidant Defenses ◽  
Seizure Threshold ◽  
Cysteine Synthase ◽  
Hyperbaric Hyperoxia

To explore the role of glutathione in protecting rats from hyperbaric hyperoxia, we administered buthionine sulfoximine (BSO) to block gamma-glutamyl cysteine synthase activity and decrease tissue glutathione synthesis. We then exposed these animals and their vehicle-treated matched controls to 100% oxygen at 4 ATA or room air at 1 ATA. After BSO treatment, glutathione concentrations in air-exposed controls decreased 62% in lung, 76% in liver, 28% in brain, and 62% in plasma. Paradoxically, BSO-treated rats were protected from hyperbaric hyperoxia. The BSO-treated animals seized significantly later and had a markedly prolonged time of survival compared with the vehicle-treated controls. We conclude that BSO treatment protects rats from hyperbaric hyperoxia, despite its effects of lowering plasma and tissue glutathione concentrations. This protection may be related to a direct effect of the compound in decreasing free radical-mediated tissue injury, increasing tissue antioxidant defenses, or increasing seizure threshold.

Free Radicals in Down's Syndrome, Amyotrophic lateral sclerosis & Rheumatoid Arthritis

2017 ◽  
Author(s):  
Luke Sammut
Keyword(s):  
Rheumatoid Arthritis ◽  
Amyotrophic Lateral Sclerosis ◽  
Free Radicals ◽  
Free Radical ◽  
Transition Metals ◽  
Tissue Injury ◽  
Down's Syndrome ◽  
Down’S Syndrome ◽  
Antioxidant Defences ◽  
Lateral Sclerosis

A free radical is an atom or group of atoms that have one or more unpaired electrons that can be considered as fragments of molecules and which are generally very reactive. Free Radicals can have positive, negative or neutral charge. They are produced continuously in cells either as accidental by-products of metabolism or deliberately during, for example, phagocytosis. The most important reactants in free radical biochemistry in aerobic cells are oxygen and its radical derivatives (superoxide and hydroxyl radical), hydrogen peroxide and transition metals. Cells have developed a comprehensive array of antioxidant defences to prevent free radical formation or limit their damaging effects. These include enzymes to decompose peroxides, proteins to sequester transition metals and a range of compounds to ‘scavenge’ free radicals. Reactive free radicals formed within cells can oxidise biomolecules and lead to cell death and tissue injury. Establishing the involvement of free radicals in the pathogenesis of a disease is extremely difficult due to the short lifetimes of these species. We describe the role of free radicals in Down's syndrome, Amyotrophic lateral sclerosis and Rheumatoid arthritis.

Prospects for treatment of free radical-mediated tissue injury

1993 ◽  
Vol 49 (3) ◽  
pp. 700-718 ◽  
Author(s):  
U Rangan ◽  
G B Bulkley
Keyword(s):  
Free Radical ◽  
Tissue Injury

scholarly journals Free-radical mechanisms in tissue injury

1984 ◽  
Vol 222 (1) ◽  
pp. 1-15 ◽  
Author(s):  
T F Slater
Keyword(s):  
Free Radical ◽  
Tissue Injury

Free radical mechanisms of tissue injury

1994 ◽  
Vol 17 (4) ◽  
pp. 373
Keyword(s):  
Free Radical ◽  
Tissue Injury
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