The achievement of boar sperm in vitro capacitation is related to an increase of disrupted disulphide bonds and intracellular reactive oxygen species levels.

The aim of this work was to determine the relationship of intracellular reactive oxygen species (ROS) and the disulphide bonds established between sperm proteins with the achievement of capacitation in boar spermatozoa. With this purpose, spermatozoa were incubated in a specifically designed in vitro capacitation medium (CM) in the presence or absence of reduced glutathione (GSH). Incubation of boar spermatozoa in CM for 4 h significantly (p < 0.05) increased free cysteine residues, which is a marker of disrupted disulphide bonds, and also intracellular ROS levels. The addition of GSH to the medium prevented most capacitation-like changes in sperm motility, membrane lipid disorder, mitochondrial membrane potential, intracellular calcium levels and localization of tyrosine-phosphorylated proteins (pTyr), but not in tyrosine phosphorylation of P32. These effects were accompanied by the inhibition of the ability of sperm cells to trigger the acrosome exocytosis in response to progesterone. When GSH was added together with progesterone after 4 h of incubation, acrosome exocytosis was not altered, but the subsequent decrease in intracellular calcium observed in controls cells was inhibited. Furthermore, co-incubation of oocytes with spermatozoa previously incubated in CM in the presence of GSH for 4 h significantly (p < 0.05) increased the number of spermatozoa attached to the oocyte surface but decreased normal fertilization rates. Our results suggest that boar sperm capacitation is related to an increase in disrupted disulphide bonds and intracellular ROS levels and that both events are related to the regulation of hyperactivated motility, intracellular calcium dynamics, sperm binding ability to the oocyte and achievement of proper nuclear decondensation upon oocyte penetration.

Surgical treatment of secundum atrial septal defect in patients older than 50 years.

BACKGROUND: The aim of this study was to verify if surgery is beneficial for patients older than 50 years. METHODS: Sixty-five patients older than 50 years were operated for a secundum atrial septal defect between November 1974 and November 1998. Preoperative data were obtained from hospital records; postoperative data from written questionnaires or direct telephone interviews. A comparison of pre and postoperative data was possible in 53 patients. RESULTS: The operative mortality was 0%. One patient died of a thromboembolic complication 32 days after surgery. The mean follow-up was 9 +/- 6 years. After surgery, clinical improvement occurred in 22 patients (41.5%) with the majority of them (69.8%) being asymptomatic or only mildly symptomatic. The occurrence of atrial fibrillation/flutter did not decrease after surgery (39.6 vs 26.4%). A thromboembolic event occurred in 2 patients before surgery and in 2 patients postoperatively; all of them had supraventricular arrhythmias and were not taking anticoagulants. CONCLUSIONS: Surgical closure of atrial septal defects in patients older than 50 years is feasible. The mortality is low. In this age group, surgery has a beneficial effect on the clinical status of the patients but not on the occurrence of supraventricular arrhythmias that can affect morbidity and mortality in patients who are not treated with anticoagulants.

[Late-appearing cholestatic icterus after a month of treatment with ticlopidine]. / Ittero colestatico a comparsa ritardata dopo trattamento per un mese con ticlopidina.

A 65-year-old man was submitted to coronary angioplasty and stent implantation for stable angina. The treatment included a 30-day therapy with ticlopidine (in addition to aspirin, metoprolol, ramipril, amlodipine and nitrates). One month after ticlopidine withdrawal a progressive cholestatic jaundice took place. Viral, immunogenic as well as nutritional causes were ruled out. The abdominal echography disclosed a normal biliary tree and the liver biopsy showed a centrolobular cholestasis pattern. Drug-induced cholestatic reaction was diagnosed and attributed to ticlopidine. There was a progressive improvement in clinical and laboratory findings 4 months after steroid treatment. The clinical picture was normalized after 6 months. When considering the option ticlopidine, even for a short time after coronary angioplasty, the possibility of drug-induced hepatotoxicity should be kept in mind. Consequently, markers of liver toxicity should be monitored carefully.