Cigarette smoking by the male partner adversely affects assisted reproductive techniques, suggesting that it may damage sperm chromatin/DNA and consequently embryo development. The effects of graded concentrations of research cigarettes smoke extract (CSE) on motility, mitochondrial membrane potential (MMP), chromatin integrity and apoptosis were evaluated in spermatozoa obtained from 13 healthy, non-smoking men with normal sperm parameters, by flow cytometry. CSE suppressed sperm motility in a concentration- and time-dependent manner and increased the number of spermatozoa with low MMP, the main source of energy for sperm motility. In addition, CSE had a detrimental effect on sperm chromatin condensation and apoptosis. Indeed, it increased the number of spermatozoa with phosphatidylserine externalization, an early apoptotic sign, and fragmented DNA, a late apoptotic sign, in a concentration- and time-dependent manner. These effects of CSE were of similar or even greater magnitude to those obtained following incubation with tumour necrosis factor-alpha, a cytokine known for its negative impact on sperm function, used as positive control. Since transmission of smoking-induced sperm DNA alterations has been found in pre-implantation embryos, and this may predispose offspring to a greater risk of malformations, cancer and genetic diseases, men seeking to father a child are recommended to give up smoking.

Polycystic ovarian syndrome (PCOS) is a reproductive system disorder characterized by irregular menses, anovulation, clinical and/or biochemical signs of hyperandrogenism (hirsutism and/or acne), ovarian micropolycystic appearance and metabolic abnormalities, such as hyperinsulinaemia and obesity. The aetiopathogenesis of this syndrome is not well known. Several pathogenetic hypotheses have been proposed to explain the full array of symptoms and signs, but with elusive results. A genetic abnormality causing PCOS is supported by the observation that different members of the same family are often affected, and about half of the sisters of PCOS women have elevated serum testosterone concentrations. Therefore, the presence of gene abnormalities in women with PCOS has been widely explored in the attempt to establish whether their mutations or polymorphisms may cause PCOS. The main genes evaluated are those involved in steroidogenesis, steroid hormone effects, gonadotrophin release regulation and action, insulin secretion and action, and adipose tissue metabolism. Despite the vast body of literature produced, none of the genes evaluated seems to play a key role in PCOS pathogenesis. It is likely that PCOS may represent the final outcome of different, deeply inter-related genetic abnormalities that influence each other and perpetuate the syndrome.

The aim of this study is to evaluate whether penile peak systolic velocity (PSV) varies in patients with erectile dysfunction (ED) due to artery insufficiency associated with abnormalities in other arterial districts or not. To accomplish this, cavernous artery PSV was determined 10, 20 and 30 min after intracavernously administering alprostadil by means of echo-color Doppler to a total of 65 consecutive patients (age range 52-78 years). In all, 18 patients had ED alone (group A) and served as controls, 15 had ED plus atheroma plaques and/or marked intima-media thickness of the common carotid artery (group B); 17 had ED plus lower limb artery abnormalities; 17 had ED plus carotid and lower limb artery abnormalities (group D). Group B and C patients had a similar PSV, which turned out to be significantly lower than that in group A. Group D patients had the lowest PSV, which proved to be significantly lower than that in groups A, B and C. This study shows that a more generalized peripheral atherosclerotic process is associated with a severer penile artery insufficiency. Therefore, ED patients with a severe arterial insufficiency should undergo an extensive echo-duplex examination.