Oxidative stress results from the imbalance between production of the reactive oxygen species (ROS) and the protective effect of the antioxidant system responsible for their neutralization and removal. An excess of ROS causes a pathological reaction resulting in damage to cells and tissues. Spermatozoa are particularly vulnerable to the harmful effects of ROS. Oxidative stress affects their activity, damages DNA structure, and accelerates apoptosis, all of which consequently decrease their numbers, hinders motility and development of normal morphology, and impairs function. This leads to disturbances in fertility or embryo development disorder. The main cellular source of ROS in the semen are immature sperm cells and white blood cells. The increase in the number of leukocytes may be due to infection and inflammation, but can also be secondary to harmful environmental factors, long sexual abstinence, or varicocele. The protective antioxidant system in the semen is composed of enzymes, as well as nonenzymatic substances, which closely interact with each other to ensure optimal protection against ROS. Non–enzymatic antioxidants include vitamins A, E, C, and B complex, glutathione, pantothenic acid, coenzyme Q10 and carnitine, and micronutrients such as zinc, selenium, and copper. It seems that a deficiency of any of them can cause a decrease in total antioxidant status. In vitro and in vivo that studies demonstrate many antioxidants possess a beneficial effect on fertility and, therefore, their use is recommended as supportive therapy for the treatment of infertility in men.

IntroductionChronic diseases such as cancer have a strong influence on both physical health and quality of life, which together comprise the concept of health-related quality of life (HRQoL) – in other words, the complete state of physical, social, and psychological functioning. Herein, we review the literature on the theory of HRQoL in relation to oncological diseases.Material and methodsA literature search of English-language publications that included an analysis of the conceptual models of HRQoL was performed using PubMed. The data were screened and synthesized by all authors and relevant papers were selected.ResultsWe outline the theoretical models most often used to conceptualize HRQoL, including the Centre for Health Promotion model from the University of Toronto, the conceptual model of Wilson and Cleary and the contextual model of Ashing-Giwa formulated specifically for cancer patients.ConclusionsUnderstanding the theoretical basis of HRQoL is indispensable for valid research in this area.

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BackgroundProstate cancer (PCa) and colorectal cancer (CRC) are the most commonly diagnosed cancers and cancer-related causes of death in Poland. To date, numerous single nucleotide polymorphisms (SNPs) associated with susceptibility to both cancer types have been identified, but their effect on disease risk may differ among populations.MethodsTo identify new SNPs associated with PCa and CRC in the Polish population, a genome-wide association study (GWAS) was performed using DNA sample pools on Affymetrix Genome-Wide Human SNP 6.0 arrays. A total of 135 PCa patients and 270 healthy men (PCa sub-study) and 525 patients with adenoma (AD), 630 patients with CRC and 690 controls (AD/CRC sub-study) were included in the analysis. Allele frequency distributions were compared with t-tests and χ2-tests. Only those significantly associated SNPs with a proxy SNP (p<0.001; distance of 100 kb; r2>0.7) were selected. GWAS marker selection was conducted using PLINK. The study was replicated using extended cohorts of patients and controls. The association with previously reported PCa and CRC susceptibility variants was also examined. Individual patients were genotyped using TaqMan SNP Genotyping Assays.ResultsThe GWAS selected six and 24 new candidate SNPs associated with PCa and CRC susceptibility, respectively. In the replication study, 17 of these associations were confirmed as significant in additive model of inheritance. Seven of them remained significant after correction for multiple hypothesis testing. Additionally, 17 previously reported risk variants have been identified, five of which remained significant after correction.ConclusionPooled-DNA GWAS enabled the identification of new susceptibility loci for CRC in the Polish population. Previously reported CRC and PCa predisposition variants were also identified, validating the global nature of their associations. Further independent replication studies are required to confirm significance of the newly uncovered candidate susceptibility loci.

There is a theory that the more evident clinical signs of testicular dysgenesis, the more frequent the neoplastic lesions are. The aim of this study was to relate the incidence of testicular germ cell neoplastic lesions (overt germ cell tumours--GCT or testicular carcinoma in situ) to the intensity of testicular organogenesis disturbances (dysgenesis). Biopsies were taken from 154 testes of the following patients: 23 patients with GCT in the contralateral gonad (CGCT), 41 patients with undescended testes operated in childhood (UDT), 90 with azoo-/oligozoospermia (A/O) diagnosed because of infertility. Assessment of seminiferous epithelium, number of Leydig cells, areal fraction of intertubular space (IS), morphometric analysis of seminiferous tubules diameter and thickness of tubular wall were performed. Monoclonal antibodies against placental like alkaline phosphatase and cytokeratin 18 were applied. Germ cell neoplastic lesions were detected in 7.1% of testes and were associated with disturbed spermatogenesis. Among testes with disturbed spermatogenesis they were found the most frequently in CGCT (22.2% vs. 11.1% in UDT and 3.8% in A/O), where spermatogenesis had the highest score (5.7 +/- 3.8 points vs. 4.2 +/- 2.7 in UDT and 4.6 +/- 2.9 in A/O). In CGCT, signs of testicular dysgenesis were less advanced: the highest tubular diameter was 164.4 +/- 32.3 microm vs. 163.5 +/- 28.6 in UDT and 161.4 +/- 31.5 in A/O, the lowest thickness of tubular wall was 8.9 +/- 3.2 microm vs. 10.2 +/- 3.6 in UDT and 10.2 +/- 3.2 in A/O, lowest IS was 36.9 +/- 14.9% vs. 47.9 +/- 18.0 in UDT and 46.5 +/- 18.5 in A/O, and the lowest percentage of tubules with immature Sertoli cells was 0.1 +/- 0.4% vs. 4.9 +/- 7.0 in UDT and 5.2 +/- 9.7 in A/O. Results indicate that neoplastic lesions appear only in testes with disturbed spermatogenesis. Worse condition of spermatogenesis is associated by the presence of other dysgenetic features, but neoplastic lesions appear more frequently in testes with the less advanced features of testicular dysgenesis.