ACS, ACLS and PLA₂ activities were detected in guinea-pig endometrium on both 7 (day of low PGF_2α output) and day 15 (day of high PGF_2α output) of the oestrous cycle and in the endometrium of ovariectomizd guinea-pigs treated with oestradiol and/or progesterone. Treatment with aristolochic acid (ARA) and quinacrine (QUIN) (PLA₂ inhibitors) significantly (P ¸0.05) reduced PG_2α output from both day 7 and day 15 endometrium cultured for 24 h, demonstrating the crucial role that PLA₂ plays in the regulation of AA release for PGF_2α synthesis in the guinea-pig. Unexpectedly, treatment with p-hydroxymercuribenzoic acid (HMB0 and thimerosal (THM) (ACS and ACLS inhibitors) also significantly (P < 0.05) decreased PGF_2α output. However, during long term inhibition of ACS and ACLS, since the rate of uptake of AA into lysophospholipids will be reduced, the amount of AA appropriately placed in the sn-2 position of appropriate phospholipids for the action of PLA₂ will also be reduced. Therefore, PLA₂ may be indirectly inhibited by a lack of substrate. ACS, ACLS and PLA₂ activities were detected in the endometrium and conceptus of early pregnant (day 15) guinea-pigs. All three enzymes were also detected in the endometrium, chorio-allantoic placenta, chorion and amnion of day 29 and 36 pregnant guinea-pigs. Treatment with THM and ARA of day 22, 29 and 36 pregnant guinea-pig endometrial and fetal tissues during 24 h culture suggested that the control of AA uptake is important in the maternal placenta, fetal placenta, chorion and amnion, and that PLA₂ appears to have an essential role in the control of PG synthesis from the endometrium, chorion and amnion of pregnant guinea-pigs. ACS, ACLS and PLA₂ may have a role in the control of arachidonic acid turnover, and therefore PG production, in guinea-pig uterine and fetal tissues. The stimulus responsible for increased PLA₂ activity towards the end of the cycle, and the mechanism of the anti-luteolytic factor provided by the guinea-pig conceptus, remains obscure. The control of AA uptake in the placenta and fetal membranes seems to have a role in the delicate regulation of PG synthesis during pregnancy.