Alexander (1979) has invited “. . . biologists to contribute to the analysis of human behavior on all legitimate fronts. . .” He considered it “. . . especially relevant that [they] take up the problem of relating human attributes to evolutionary history.” The analysis of human sexual behavior surely qualifies as a legitimate topic in evolutionary biology. This chapter represents a contribution to the argument that sperm competition does occur in humans and has been a selective force in the evolution of certain human characteristics. There has been considerable controversy over what may be the “natural” sexual inclinations (promiscuous, polygynous, serially polygynous, monogamous, or some mixture of these) of human males (e.g., Trivers 1972; Wilson 1975; Alexander 1977; Short 1977, 1979, 1981; Daly and Wilson 1978; Symons 1979; Lovejoy 1981; Barash 1982; Harvey and Harcourt, this volume), but relatively much less debate over the sexual predilections of human females (Hrdy 1981). Females are widely assumed to be monogamous, with little formal recognition of alternative female strategies (but see Hrdy 1981, and Knowlton and Greenwell, this volume). The compromise view of human male mating strategy proposes mixed tactics (Trivers 1972) where males attempt to pair-bond with one or more females by high investment, and opportunistically (more or less promiscuously) mate with other females. All combinations of male tactics from rape (Shields and Shields 1983, Thornhill and Thornhill 1983) to high investment (Trivers 1972) and the environmental and social circumstances that occasion their expression have received analysis in the literature. As Hrdy (1981) observed: “The sociobiological literature stresses the travails of males – their quest for different females, the burdens of intra-sexual competition, the entire biological infrastructure for the double standard. No doubt this perspective has led to insights concerning male sexuality. But it has also

19 – Human Sperm Competition

Boyden,S.V. 1 9 6 2 . The c h e m o t a c t i c e f f e c t of m i x t u r e s of an t ibody and a n t i g e n on polymorphonuclear l e u c o c y t e s . J.ISxp. Med. 115:453. Bygdeman,M.,B. F red r i c s son ,K . Svanborg and B . Sarnuelsson 1970. The r e l a t i o n between f e r t i l i t y and p r o s t a g l a n d i n cont e n t of s emina l f l u i d i n man. F e r t i 1 . a n d S t e r i l . g : 6 2 2 . Crunkhorn,P. and A . L . W i l l i s 1 9 7 1 . Cutaneous r e a c t i o n s t o i n t r a d e r m a l p r o s t a g l a n d i n s . Bri t .J .Pharmaco1. 4 1 : 4 9 . E r i c s s o n , R . J . 1970. Leucocytes and sperm c a p a c i t a t i o n . J. Reprod.Fert .Supp1. g : 1 4 7 . G i roud , J .P . and D.A. Willoughby 1970. The i n t e r r e l a t i o n s of complement and a p r o s t a g l a n d i n l i k e s u b s t a n c e i n a c u t e inf lammation. J .Pa tho1 . 101: 241. Kaley & Weiner: Inflammatory Response 349 Hirsch,J.G. and A.B. Church 1960. Studies of phagocytosis of group A streptococci by polymorphonuclear leucocytes -in vitro. J.Exp.Med. =:309. Horton,E.W. 1963. Action of prostaglandin E l on tissues which respond to bradykinin. Nature,z:892. Horton,E.W. 1969. Hypotheses on physiological roles of prostaglandins. Physiol.Rev. 49:122. Hurley,J.V. and W.G. Spector 1961. Endoqenous factors responsible for leucocyte emigration in vivo. J.Pathol.and Bacteriol. 82: 403. Kaley,G. and R. Weiner 1968. Microcirculatory studies with prostaglandin El. In: Prostaglandin Symp.Worcester Found. Exp.Biol.(P.W. Ramwell & J.E. Shaw,eds.). Interscience,N.Y. p.321. Keller,H.U. and E. Sorkin 1967. Studies on chemotaxis. VI. Specific chemotaxis in rabbit polymorphonuclear cells and mononuclear cells. 1ntern.Arch. Allergy 31:575. Konijn,T.II.,J.G.C. van de Meene,J.T. Bonner and D.S. Barkley 1967. The acrasin activity of adenosine 3',5'-cyclic phosphate. In: Proc.Nat'l.Acad.Sci. U.S. 2:1152. Laity,J.L. 1970. The effect of histamine releasers on the output of prostaglandins from rat diaphragms. J.Pharm. Pharmacol . 2: 3 8 4. Macmorine,D.R.L.,H.Z. Movat,R. Neta and Y. Takeuchi 1968. In vitro release of permeability factors and a slow reacting substance from phagocytising PMN-leucocytes. In: Fed.Proc. 27:249 (Abstract) . Majno,G.,G.E. Palade and G.I. Schoefl 1961. Studies on inflammation. 11. The site of action of histamine and serotonin along a vascular tree: A topographic study. J.Biophys. Biochem.Cyto1. 11: 607. Mannaioni,P.F. 1970. Influence of bradykinin and prostaglandin El on the uptake and release of histamine by murine neoplastic mast cells in vitro. Biochem.Pharmaco1. 2:1159. Miles,A.A. and D.L. Wilhelm 1955. Enzyme-like globulins from serum reproducing the vascular phenomena of inflammation. I. An active permeability factor and its inhibitor in guinea-pig serum. Brit.J.Exp.Patho1. 2:71. 14oses,J.M.,R.H. Ebert,R.C. Graham and K.L. Brine 1964. Pathogenesis of inflammation. I. The production of an inflammatory substance from rabbit granulocytes in vitro and its relationship to leucocytic pyrogen. J.ExKMed.20:57. Movat,H.Z. 1971. Personal communication. -350 Annals New York Academy of Sciences Norton,S. 1954. Quantitative determination of mast cell fragmentation by compound 48/80. Brit.J.Pharmaco1. 9:494. Piper,P.J. and J.R. Vane 1969. Release of additional factors in anaphylaxis and its antagonism by anti-inflammatory drugs. Nature,=:29. Ratnoff,O.D. and I.H. Lepow 1963. Complement as a mediator of inflammation. Enhancement of vascular permeability by purified human C'1 esterase. J.Exp.Med. =:681. Scott,R.E. 1970. Effects of prostaglandinsfepinephrine and NaF on human leucocyte,platelet and liver adenyl cyclase. Blood, 35: 514. S#ndergaard,J. and M.W. Greaves 1970. Recovery of a pharmacologically active fatty acid from human allergic contact eczema using a skin perfusion method. In: Fed-Proc. 2:419 (Abstract). Soupart,P. 1970. Leucocytes and sperm capacitation in the rabbit uterus. Ferti1.and Steril. z:724. Spector,W.G. and D.A. Willoughby 1963. The inflammatory response. Bact.Rev. 2: 117. Ward,P.A. 1970. Neutrophil chemotactic factors and related clinical disorders. Arth.and Rheum. 2:181. Ward,P.A. ,C.G. Cochrane and H.J. Muller-Eberhard 1965. The role of serum complement in chemotaxis of leucocytes & vitro. J.Exp.Med. =:327. Weiner, R. 1968. Vascular reactions to prostaglandin El in rat mesentery,cremaster muscleland skin. In: Proc. 5th Europ.Conf.Microcirculation. p.157. Willis,A.L. 1969. Parallel assay of prostaglandin-like activity in rat inflammatory exudate by means of cascade superfusion. J.Pharm.Pharmaco1. 2: 126.

Prostaglandin e1: a potential mediator of the inflammatory response

ALMOST 30 years after the initial discovery of the prostaglandins, Bergstrom et al., succeeded in isolating and identifying prostaglandins (PGs) E1, E2, F1α and F2α from sources including human semen1. It was subsequently claimed2 that the 19-hydroxy derivatives of prostaglandins A and B were also present. These compounds were later found at an average concentration of 40 µg ml−1 (ref. 3), In a detailed study of semen PGs we have used a new approach for the measurement of the E prostaglandins, which involves protecting the unstable β-ketol system by oximation in the unextracted semen, thus ensuring minimal degradation to the A or B series. Using this technique we found that the levels of 19-hydroxy derivatives of PGA and PGB are relatively low whereas two new PGs, later identified as 11α,15,19-trihydroxy-9-keto prost-13-enoic acid (19-hydroxy PGE1) and 11α,15,19-trihydroxy-9-keto prosta-5,13-dienoic acid (19-hydroxy PGE2) were present at an average total concentration of 100 µg ml−1. These compounds can be isolated together as the methyl ester/methyl oxime derivatives by thin layer chromatography and the individual components can be separated by gas chromatography as the methyl ester/methyl oxime/tert-butyl dimethyl silyl ethers4.

19-HydroxyIated E prostaglandins as the major prostaglandins of human semen

The contractile response of the human uterus, fallopian tubes, and ovary to prostaglandins in vivo.

BACKGROUND: Transport of gametes and embryos is an important function of the Fallopian tube. Both muscular contractions and cilia activity are involved in the transportation. Prostaglandins (PGs) are known mediators of muscular contractility. PG receptors have previously been demonstrated in the human Fallopian tube. The aim was to study the effect of PGs and progestagens, antiprogestin, hCG and oxytocin on muscular contractions in the human Fallopian tube, and the hormonal regulation of PG receptors. METHODS: Twenty-two healthy women operated for benign causes were included in the study. The ampullary-isthmic junction of the Fallopian tubes was excised and used for in vitro contractility studies. The effect of PGE(1), PGE(2), PGF(2alpha), progesterone, mifepristone, levonorgestrel, oxytocin and hCG on contractility was studied. Explants of Fallopian tubes were cultured for 24 h to study the effect of progestagens and hCG on the expression of PG receptors using immunohistochemistry and real-time PCR. RESULTS: Muscular contractions increased after treatment with PGF(2alpha) and PGE(2) (P < 0.05). The contractions decreased after PGE(1), progesterone, levonorgestrel, mifepristone, oxytocin and hCG (P < 0.05). In tubal explant studies, relative mRNA expression of EP1, EP2, EP3 and FP increased after levonorgestrel treatment (P < 0.05). Mifepristone and levonorgestrel treatment increased immunostaining intensity of EP1 and EP2 protein, in lumen, muscle and vessels. Progesterone and mifepristone increased immunostaining of FP in vessels. CONCLUSIONS: These data suggest that the transport of gametes and embryos involves the action of PGs, progesterone, oxytocin and hCG on muscular contractility.

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K. Svanborg

Papers

The Relation Between Fertility and Prostaglandin Content of Seminal Fluid in Man