Quantification of the scavenger capacity of different flavonoids with regard to the superoxide ion.
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Biomedical subjects
Publications and source records attributed to N Darmon.
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We describe a patient undergoing long-term hemodialysis, in whom severe chondrolysis of the hip joint developed. The chondrolysis evolved in the absence of synovial inflammation and articular chondrocalcinosis. Biochemical studies of articular cartilage retained at surgery revealed deposition of exclusively small proteoglycans in the matrix. This may have been an important factor leading to the rapid chondrolysis in this patient.
A polyethylene sheet was implanted in the patellofemoral joint of the right knee of the rabbit and the biochemical and metabolic changes in the articular cartilage from femoral trochleas (in contact with the implant) and femoral condyles (free of direct contact) were compared with those in their sham-operated counterparts 7, 15, and 30 days after joint implantation. The results showed that there was an increase in the water content; the extraction yields of uronic acid--, 35SO4-, and [3H]glycine-containing compounds; and the incorporation of [3H]thymidine, [3H]glycine, and 35SO4. Concomitantly, the contents of uronic acid--, hexosamine-, neutral sugars-, and hydroxyproline-containing substances decreased in the femoral trochlear cartilage and, to a much lesser extent, in the femoral condylar cartilage from implanted joints. The increased capacity of viable chondrocytes to incorporate metabolic radiolabeled precursors into newly synthesized macromolecules may represent a reparative cell response to the tissue injury induced by the implant. This is therefore a useful model for studying the response of chondrocytes to mechanical injury and tissue tolerance to intraarticularly implanted prosthetic materials.
The effect of various anti-inflammatory drugs on the production of prostaglandins E2 and F2 alpha, 6 keto PGF1 alpha and thromboxane B2 by bovine articular chondrocytes was measured by radioimmunoassay. While indomethacin and meclofenamic acid caused a dose-dependent inhibition of all prostanoids measured, the effects of hydrocortisone and colchicine varied with respect to different prostanoids. Hydrocortisone (10(-7)M - 10(-13)M) both in the presence and absence of added arachidonic acid, resulted in an inhibition of prostaglandins E2 and F2 alpha, and to a lesser extent, 6 keto PGF 1 alpha, but TxB2 production was only slightly inhibited by the drug in the absence of arachidonic acid and markedly increased in its presence. Colchicine (10(-7)M-10(-3)M) had the opposite effect, causing an inhibition of TxB2 and stimulating PGE2 and 6 keto PGF1 alpha production. These findings suggest that certain anti-inflammatory drugs may, in addition to their action on phospholipase A2 and cyclo-oxygenases, exert potent effects at the level of the different synthetases. In order to see whether these alterations in relative prostanoid levels affected proteoglycan metabolism, the effect of anti-inflammatory drugs on proteoglycan synthesis by cultured chondrocytes was tested using 35SO4 labeling methodology. The results showed that at the concentrations tested (10(-5)M to 10(-7)M), indomethacin, dexamethasone, hydrocortisone and colchicine inhibited 35SO4 incorporation into newly synthesized proteoglycan molecules both in the presence (10(-6)M) and absence of exogenous arachidonic acid. In the same concentration range chloroquine had no effect. These results do not support the hypothesis of direct prostanoid involvement in the modulation of proteoglycan synthesis in articular cartilage.
The joint tissues (synovium, articular cartilage and bone), respond rapidly and consistently to the presence of a piece of polypropylene surgically implanted into the Rabbit knee joint. In the contact of a foreign body, a synovium proliferates in an attempt to isolate and exclude the intruder from the joint cavity. The articular cartilage degenerates at the sites of maximal pressure. Its superficial layer undergoes cell necrosis and fibrillation and is progressively destroyed in the process of mechanical grinding. At the sites of lower pressure, the chondrocytes proliferate and form the metabolically hyperactive clones which have increased capacity to incorporate tritiated thymidine and radioactive sulfate. The glycosaminoglycan content of articular cartilage, compared to the shamoperated control side, rapidly decreases after operation as suggested by a loss of metachromatic staining and lower per unit weight concentration of uronic acid and hexosamine. In addition to the above changes, the osteophytes quickly develop at the articular margins from the proliferating synovial tissue while underlying bone become thicker and eburnated. These foreign body induced changes in articular morphology and metabolism resemble closely those observed in osteoarthrosis. The present model therefore may prove useful in studying the latter condition.