Problems connected with in vivo labelling of embryonic glycosaminoglycans with Na2 35SO4 in teratological studies

Decrease of inorganic blood sulfate following treatment with selected antirheumatic drugs: Potential consequence for articular cartilage

“…Not unexpected, the salicylate derivatives aspirin, diflunisal and benorylate, the latter is a conjugate of paracetamol and aspirin, provoke a decrease of inorganic sulfate in the circulation. We presume that the mechanism of action is similar to that of sodium salicylate, a drug which decreases serum sulfate in rats [4] and mice [3], by an unknown mode of action on the kidney, causing sulfate diuresis. The observed delay in action of the salicylate derivatives compared to that of sodium salicylate, could be explained by differences in absorption-rate kinetics or by the time lost for biotransforming (via hydrolysis) these agents to the active moiety, which possesses structures resembling the conjugated ct-keto-enol system of salicylate.…”

“…Some drugs are reported to modulate the 35 S kinetics (tracer given as 35SO~) in rat serum, as there are vitamin A, tolbutamide and triiodothyronine [4]. Sulfaturic effects have been attributed to calcitonin [28], a small peptide with analgesic [29] and antiphlogistic properties [30]; indeed high doses of sodium chloride are capable to exert sulfate diuresis in dogs and rats [31,27].…”

“…In mice, sodium salicylate decreases the level of inorganic sulfate by another process, i.e. sulfate diuresis [3], which is also the cause of the same phenomenon seen in salicylate treated rats [4,5]. A potential consequence of a reduced sulfate availability may be a suppression of biosynthesis of the highly sulfated proteoglycans, abundantly present in fetal skeletal tissue and cartilage, as was shown in mice and rats [3,6,7], leading ultimately to inferior tissue properties.…”