Abstract
Borgeat and Sirois (1) have summarized the relationship between arachidonic acid (20:4) metabolites and lysosomal enzyme release thusly: agents which increase cellular levels of cAMP inhibit lysosomal enzyme release, whereas agents which increase cGMP induce release. In 3T3L1 fibroblasts the most potent stimulator of increased cAMP is PGI2 followed by PGE1 (2). However, the relative potency of the prostaglandins for cAMP accumulation appears to be a function of the cell type. Thromboxane A2 prevents an increase in cellular cAMP due to an external stimulus (3). In contrast to the cyclooxygenase products (PGI2, PGE1, etc.), products of the lipoxygenase pathway have been shown to increase cellular cGMP (4).
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© 1985 Martinus Nijhoff Publishing, Boston
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Sloane, B.F., Honn, K.V. (1985). Proteolytic Enzymes and Arachidonic Acid Metabolites. In: Lands, W.E.M. (eds) Biochemistry of Arachidonic Acid Metabolism. Prostaglandins, Leukotrienes, and Cancer, vol 1. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2597-0_19
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DOI: https://doi.org/10.1007/978-1-4613-2597-0_19
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