Boar and human sperm as cellular models for membrane phospholipid biosynthesis and degradation

Boar sperm phospholipids are enriched in long chain polyunsaturated fatty acids, especially 22:5(n-6) and 22:6(n-3); whereas, human sperm phospholipids are enriched in 22:6(n-3) with little or no 22:5(n-6) present. When boar semen was incubated with (1-14C)-arachidonic acid, spermatozoa showed an unsual ability to incorporte the label into phospholipids, particularly phosphatidylcholine. The biphasic mode of uptake suggests that arachiudonate incorporation is mediated through acyltransferase and the de novo route. Membrane active drugs were found to affect the phospholipid biosynthetic pathway. For example, catonic amphiphilic compounds such as propranolol inhibited incorporation of labeled archidonate into phosphatidylcholine and gave rise to increased radioactivity in phosphatidic acid. Although at a much lower level, labeled arachidonate was incorporated similarly into phospolipids of human spermatozoa. When prelabeled human spermatozoa were washed and reincubated in buffer, a substantial amount of labeled archidonate was released from phospholipids but not plasmalogens. Phospholipid hydrolysis was enhanced by Ca2+ and inhibited by EGTA, suggesting activation of calcium dependent phospholipase A2. The release of labeled arachidonic acid from prelabeled human sperm was affected by membrane active drugs such as propranolol. Many of the compounds which inhibit phopholipid biosynthesis and degradation also inhibit sperm motility. Consequently, boar and human spermatozoa aare good cellular models for evaluating drug effects on phospholipid metabolism and membrane function