Polycystic ovary syndrome is the most important cause of chronic anovulation. In women who fail to respond to clomiphene, low-dose FSH given in a step-wise fashion can induce normal follicular growth and ovulation. The failure of the action of endogenous FSH in these women may be related to reduced biological activity of circulating FSH, but may also involve inhibition of its action at follicular level by polypeptide growth factors such as EGF.

Follicular fluid lactate levels were measured in women undergoing infertility surgery during the follicular phase or oocyte recovery for in-vitro fertilization (IVF). In the largest ovulatory follicle lactate levels were low in the mid-follicular phase (group 1), 1.6-fold higher just prior to the onset of the luteinizing hormone (LH) surge (group 2) and a further 2.5-fold higher after the onset of the LH surge (group 3). In IVF patients mean lactate levels in all aspirated follicles were similar to those in group 3 subjects, but the levels within each patient were variable and were positively correlated with follicular volume. Basal granulosa cell lactate accumulation in vitro was 3-fold higher in group 3 compared with group 2 subjects, but stimulation by FSH or HCG was higher in group 2 (2- to 3-fold) compared with group 3 (1.4- to 2-fold). These results demonstrate that human follicular fluid lactate levels increase as a function of the maturity and size of the developing follicle. Granulosa cell lactate accumulation in vitro is under gonadotrophic control, which suggests that the effects observed in vivo reflect changes in granulosa cell glycolysis in response to gonadotrophic stimulation. Our findings support the concept that low molecular weight energy metabolites transduce gonadotrophin signals that regulate oocyte maturation.

Pentoxifylline improves some motility characteristics of human spermatozoa, but the variability of response to this drug has not been clearly defined. We used computer-assisted sperm motion analysis to examine the in-vitro response of spermatozoa to pentoxifylline. Individuals (n = 31) with normal sperm counts were randomly selected and their spermatozoa exposed to different concentrations of pentoxifylline. Further tests on a subgroup of individuals examined the longevity of spermatozoa in response to this agent. Straight line velocity (VSL) was only improved at 0.1 mM and the major effect of the drug was on curvilinear velocity (VCL) and lateral head displacement (ALH). Prolonged exposure to pentoxifylline enhanced sperm motion only at 0.1 mM. Higher concentrations produced dose-dependent detrimental effects on all the motion characteristics. There was considerable inter-individual variability in both VCL and ALH response ranging from little or no detectable response to a 40% increase above control value. The maximum response was most commonly seen at a concentration of 2 mM pentoxifylline.

Summary A comparison of the lactate dehydrogenase (LDH) isoenzyme pattern found in the red cells from patients with megaloblastic anaemia, with that of normal human red cells, and the red cells from patients with iron deficiency and haemolytic anaemias, has shown that megaloblastic anaemia, whether due to vitamin B12 deficiency, folate deficiency, or a mixed deficiency of both vitamins, causes a characteristic reversal in distribution of the faster moving isoenzymes LDH‐1 and LDH‐2. In normal red cells and those present in other anaemias, LDH‐2 activity is always greater than LDH‐1 activity, but in all cases of megaloblastic anaemias examined, LDH‐1 was consistently greater than LDH‐2 activity. This reversed LDH isoenzyme pattern is also present in the serum in megaloblastic anaemia, and is almost certainly derived from intramedullary destruction of megaloblastic precursor cells, with very little contribution from the circulatory red cells. It is well known that a feature of megaloblastic anaemia is a raised serum LDH activity, and it has been shown that a simple chloroform inhibition test made on either serum showing a raised serum LDH of over 900 units, or on the red cells, will give 2 good indication that this reversed pattern is present.

Diet has important effects on normal physiology and the potential deleterious effects of high fat diets and obesity on male reproductive health are being increasingly described. We conducted a histological review of the effects of chronic high fat (HF) diet (using a mouse model fed a 45% fat diet for 21 weeks) with a discovery proteomic study to assess for changes in the abundance of proteins in the testis. Mice on a HF diet became obese and developed glucose intolerance. Using mass spectrometry, we identify 102 proteins affected in the testis of obese mice. These included structural proteins important for the blood testis barrier (filamin A, FLNA), proteins involved in oxidative stress responses (spermatogenesis associated 20, SPATA-20) and lipid homoeostasis (sterol regulatory element-binding protein 2, SREBP2 and apolipoprotein A1, APOA1). In addition, an important regulator protein paraspeckle component 1, PSPC-1, which interacts with the androgen receptor was significantly downregulated. Proteomic data was validated using both Western blotting and immunostaining which confirmed and localised protein expression in both mouse and human testis using biopsy specimens. This study focused mainly on the abnormalities that occurred at the protein level and as a result, we have identified several candidate proteins and conducted pathway analysis around the effects of HF diet on the testis providing novel insights not previously described. Some of the identified targets could be targeted therapeutically and future work is directed in this area.