Oner Balbay

Alterations in semen parameters of toll collectors working at motorways: does diesel exposure induce detrimental effects on semen?

Air pollution is contemporarily considered to be a significant cause in impairing semen parameters. The aim of this study was to investigate possible effects of traffic pollutants, mainly the diesel exposure, on semen analysis. A total of 38 men working as toll collectors at motorways formed the study group. Simultaneously, 35 men working as office personnel constituted the control group. Factors including varicocele, chronic diseases that can affect sperm production were the exclusion criteria. No difference regarding smoking was present between the groups. Usual semen analysis according to WHO guidelines was performed. The results of semen analysis revealed decreased motility and low sperm counts in eight and seven men from the study group respectively. Besides, a man from the same group had combined abnormality of decreased motility and low sperm count. However, two men from the control group had slight motility defect and one had low sperm count. The differences regarding the abnormal sperm count and motility were significant between the groups (Pu2003=u20030.002 and Pu2003=u20030.003, respectively). Similarly, the ratio of sperm cells with normal morphology was significantly lower in the study group than that in the control group (Pu2003=u20030.001). This observation proposes that air pollution particularly diesel exposure may have detrimental effects on sperm parameters.

Erdosteine protects rat testis tissue from hypoxic injury by reducing apoptotic cell death

The purpose of this study was to examine the effects of hypobaric hypoxia on testis morphology and the effects of erdosteine on testis tissue. Caspase‐3 and hypoxia‐inducible factor 1α expressions were detected by immunohistochemistry. Adult male Wistar rats were placed in a hypobaric hypoxic chamber. Rats in the erdosteine group were exposed to the same conditions and treated orally with erdosteine (20 mg kg−1 daily) at the same time from the first day of hypoxic exposure for 2 weeks. The normoxia group was evaluated as the control. The hypoxia group showed decreased height of spermatogenic epithelium in some seminiferous tubules, vacuolisation in spermatogenic epithelial cells, deterioration and gaps in the basal membrane and an increase in blood vessels in the interstitial area. The erdosteine group showed amelioration of both epithelial cell vacuolisation and basal membrane deterioration. Numbers of hypoxia‐inducible factor 1α–immunostained Sertoli and Leydig cells were significantly higher in the hypoxia group than in the erdosteine group. The number of seminiferous tubules with caspase‐3–immunostained germ cells was highest in the hypoxia group and decreased in the erdosteine and normoxia groups respectively. Based on these observations, erdosteine protects testis tissue from hypoxic injury by reducing apoptotic cell death.

Reduced plasma fetuin-A levels in patients with obstructive sleep apnoea

To the Editors:nnObstructive sleep apnoea syndrome (OSAS) has been increasingly linked to cardiovascular disease. fetuin-A is an inhibitor of vascular calcification and an anti-inflammatory cytokine. We tested the hypothesis that plasma levels of fetuin-A are decreased in patients with OSAS.nnWe studied 119 patients with OSAS and 35 controls. Participants were recruited and studied at the sleep unit at Hospital Universitari Son Espases, Palma de Mallorca, Spain. Serum levels of fetuin-A, glucose, triglycerides, cholesterol, high-density lipoprotein (HDL) cholesterol, creatinine, aspartate aminotransferase (AST), alanine aminotransferase (ALT) and gamma glutamyltransferase (GGT) were determined.nnPlasma fetuin-A levels were significantly lower in patients with OSAS than in controls (mean±sd 368±66 versus 445±53 ng·mL−1, p=0.015). In multivariate analysis, fetuin-A levels were independently associated with OSAS (p=0.034). OSAS is associated with reduced levels of fetuin-A and fetuin-A could be one of the contributing factors for the development of cardiovascular complications in OSAS patients.nnThere is evidence that patients with OSAS have an increased risk for cardiovascular diseases [1]. The mechanisms underlying this association are unclear but candidate mechanisms include endothelial dysfunction, oxidative stress, systemic inflammation and metabolic dysregulation [2]. Vascular calcification has recently received much attention because of its relationship with cardiovascular disease [3, 4]. Chronic inflammation may promote vascular calcification and recent studies have demonstrated a relationship between vascular calcification and endothelial dysfunction [5, 6].nnFetuin-A is a circulating protein mostly synthesised in the liver [7, 8] that is known to be an important inhibitor of vascular calcification and a potent anti-inflammatory cytokine [8–10]. Fetuin-A is considered to be a mediator that links chronic inflammation to cardiovascular diseases [11]. However, previous studies investigating the role of fetuin-A in patients with cardiovascular disease …