Comparison of nervous-tissue lipid fatty acid patterns of various animal species with particular reference to docosahexaenoic acid.

during the S phase is shown in Table 1. DNA synthesis at 21-22h was inhibited; the effect was maximal when the drugs were administered at 18 h. This confirms the previous observations (Thrower & Ord, 1974a,b) of an a-adrenergic facilitation of DNA synthesis during the late S phase. The time-course of incorporation of [jHIthymidine into liver DNA after administration of phenoxybenzamine at 18h is shown in Fig. l(6). DNA synthesis at 21-22 h is decreased, and the amount of r3H]thymidine incorporated into DNA during the whole wave appears to be decreased. Table 1 compares the effects of aand 8-adrenergic-blocking drugs, administered at 18 h, on DNA synthesis and cyclic AMP production at 21-22h. As expected, phenoxy benzamine did not inhibit the increase in cyclic AMP production, since catecholamines act at 8-adrenergic sites to stimulate liver adenylate cyclase. However, the 8-blockers propranolol (lOmg/kg) and pindolol (LB 46; 5mg/kg) failed to inhibit the increase in cyclic AMP concentration; DNA synthesis at 21-22h was also unaffected by propran0101. Both aand 8-blockers, administered at 18h, caused an increased in ornithine decarboxylase activity at 21 h (control animals 195 k 68pmol of 14C02/20min per mg of protein; phenoxybenzamine-treated animals, 320 k 102; pindolol-treated animals, 340 k 14. It is clear that, at this time, 18-22h after the operation, the hormonal control of these parameters differs from that observed for the changes at M h and at 12-13 h (Thrower et al., 1973; Thrower & Ord, 1974u,b). Catecholamines still play an important role at this time, facilitating DNA synthesis in the replicating hepatocytes via a-adrenergic receptors. The increases in cyclic AMP concentration and ornithine decarboxylase activity appear to be co-ordinate, but are not regulated by catecholamines; the observed changes could be accounted for in terms of increased glucagon secretion activating liver adenylate cyclase, or decreased insulin secretion decreasing liver cyclic AMP phosphodiesterase activity: the increased concentration of cyclic AMP would also result in increased ornithine decarboxylase activity (Beck et al., 1972). The role of the increase in cyclic AMP production after 19h remains unclear. It is possible that this increase may have a function in regulating the wave of DNA synthesis, although the previous waves of cyclic AMP production at 4h and 12-13 h after partial hepatectomy do not appear to serve such a function (Thrower & Ord, 1974~).