Prostaglandin A2 and 35S uptake in connective tissue

Denko, Charles W.; Petricevic, M

doi:10.1016/0090-6980(77)90197-6

Cited by 4 publications

(5 citation statements)

References 7 publications

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“…Sex status may also be an important factor in influencing the response of copper-deficient animals to irritants. Thus Denko showed that 0.6 p.p.m, of copper in the diet was sufficient to cause, after two months of feeding, an enhanced inflammatory response in male rats [49,54], while, in female rats, the same level of copper restriction did not elicit a similar behaviour, even after five months of copper-deficiency [53].…”

Section: Copper In Acute Inflammation (A) Anti-inflammatory Activity mentioning

confidence: 93%

“…However, evidence coming particularly from studies on superoxide anion production and superoxide dismutase activity in rheumatic patients [40,41], together with the results obtained in acutely-inflamed copper-deficient rats [14, 49,53,54], led to the suggestion that any condition responsible for an enhanced production of free radicals in vivo could significantly exacerbate, if not prime, the inflammatory reaction [34]. Thus, as noted earlier for chronic inflammation, the requirement for copper in free radical metabolism may have a predominant, although not exclusive, role in explaining the activity of this metal as an acute anti-inflammatory agent.…”

Section: (D) a Possible Mechanism Of Actionmentioning

confidence: 96%

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Review: Copper and inflammation — a possible rationale for the pharmalogical manipulation of inflammatory discorders

et al. 1985

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Acute and chronic inflammations are characterized, among other features, by changes in the metabolism of copper and by a widespread responsiveness to the therapy with copper-containing molecules. The exact map of inflammation-induced copper movements as well as the role played by the metal in the pathogenesis of inflammatory disorders are, however, far from being clear, and this is especially true in the case of chronic processes. Nevertheless the present knowledge suggests that the "copper approach' may provide a new way for coping with the problem of anti-inflammatory/anti-arthritic therapies. The administration of exogenous copper, and the in vivo manipulation of the endogenous metal levels are proposed as two possible therapeutic strategies, not necessarily mutually exclusive. For a better understanding of the value of such an approach, further research work is needed, especially to attain a more detailed know-how on the involved chemical forms, distribution and functions of copper in both normal as well as inflamed organisms.

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Section: Copper In Acute Inflammation (A) Anti-inflammatory Activity mentioning

confidence: 93%

Section: (D) a Possible Mechanism Of Actionmentioning

confidence: 96%

Review: Copper and inflammation — a possible rationale for the pharmalogical manipulation of inflammatory discorders

et al. 1985

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“…However, no significant differences in edema were found between normally fed and copperdeficient rats when the latter were kept on a diet containing 0.6-0.8 #g of copper/g of diet and distilled-deionized water for as long as 5 months. In contrast to the above results, DENKO et al [5] reported that rats kept on a diet containing 0.6/~g of copper/g of diet and tap water (containing 1.5 /~g of copper/ml) for only 2 months developed significantly more edema than rats given a normal diet and tap water. Whereas these results demonstrate that the effects of copper deficiency on inflammation are probably influenced by strain, sex, model of inflammation, and length of copper deprivation, the actual tissue levels of copper at the time of assay may be most critical.…”

Section: Introductionmentioning

confidence: 57%

“…It is, therefore, likely that zinc and iron also play important roles in inflammation. It has been reported that rats fed a diet low in zinc developed more carrageenin-induced paw edema [5] but less adjuvant-induced polyarthritis [2] than controls fed a normal diet. In view of these observations we also analyzed plasma and tissues for zinc and iron.…”

Section: Introductionmentioning

confidence: 99%

“…During the past few years a number of reports have appeared regarding the role of dietary copper in animal models of inflammation [1][2][3][4][5]. MILANINO and co-workers [1] found a strong inhibition of adjuvant arthritis when 25-30 day old female Sprague-Dawley rats were fed a copper-deficient diet (0.4 pg of copper/g of diet; 5 pg of copper/g of diet provides adequate copper intake in the rat) and distilled-deionized water for 2 months.…”

Section: Introductionmentioning

confidence: 99%

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Effect of nutritional copper deficiency on adjuvant arthritis and immunocompetence in the rat

et al. 1984

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Both severe and marginal copper deficiency were produced in male Sprague Dawley rats prior to induction of adjuvant arthritis. Degree of copper deficiency was confirmed by analysis of plasma, liver, and brain samples prior to adjuvant injection. Incidence of adjuvant arthritis was the same in both copper deficient and control animals although the severity was slightly but not statistically less in the former. However, recovery from foot edema was impaired in copper-deficient animals, while marginally copper-deficient animals recovered at the same rate as did controls. Plasma copper concentration increased in response to the injection of adjuvant and the increase was directly related to dietary copper content. Plasma zinc concentration was decreased in arthritic animals and the decrease was inversely correlated to paw edema. Liver copper, zinc, and iron concentrations in arthritic animals remained unchanged or increased slightly in comparison to the corresponding non-injected controls. Copper-deficient rats were immunosuppressed as demonstrated by impaired responsiveness to the T-cell dependent contact sensitizing agent oxazolone and diminished capacity to respond to the T-cell independent antigen Type III pneumococcal polysaccharide. Although a statistical difference in paw volumes was not found for group of animals fed diets differing in copper content, it is postulated that copper deficiency may alter the severity and kinetics of adjuvant arthritis by impairing aspects of the immune response and the tissue repair processes subsequent to injury.

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Beta-endorphin, immunological and biochemical changes in synovial fluid in rheumatic disorders

et al. 1986

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In 120 patients with rheumatic disorders concomitant assays of serum and synovial fluid were done for acute phase reactants, immunoglobulins and the neuropeptide beta-endorphin. One-third of the patients with rheumatoid disease demonstrated synovial fluid levels of endorphin to be several-fold higher than serum levels, while in two-thirds the opposite results were found. These changes are discussed as adaptive or defense mechanisms. The synovial membrane is postulated to synthesize beta-endorphin.

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Prostaglandin A2 and 35S uptake in connective tissue

Cited by 4 publications

References 7 publications

Review: Copper and inflammation — a possible rationale for the pharmalogical manipulation of inflammatory discorders

Review: Copper and inflammation — a possible rationale for the pharmalogical manipulation of inflammatory discorders

Effect of nutritional copper deficiency on adjuvant arthritis and immunocompetence in the rat

Beta-endorphin, immunological and biochemical changes in synovial fluid in rheumatic disorders

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