This work aimed to assess the relationship of seminal ascorbic acid levels with smoking in infertile males. One hundred and seventy men were divided into four groups: nonobstructive azoospermia [NOA: smokers (n = 20), nonsmokers (n = 20)]; oligoasthenozoospermia [smokers (n = 30), nonsmokers (n = 20)]; asthenozoospermia [smokers (n = 20), nonsmokers (n = 20)] and normozoospermic fertile men [smokers (n = 20), nonsmokers (n = 20)]. The patients underwent medical history, clinical examination, conventional semen analysis and estimation of ascorbic acid in the seminal plasma calorimetrically. There was a significant decrease in the mean seminal plasma ascorbic acid levels in smokers versus nonsmokers in all groups (mean +/- SD; 6.03 +/- 2.18 versus 6.62 +/- 1.29, 7.81 +/- 1.98 versus 9.44 +/- 2.15, 8.09 +/- 1.98 versus 9.95 +/- 2.03, 11.32 +/- 2.15 versus 12.98 +/- 12.19 mg dl(-1) respectively). Fertile subjects, smokers or not, demonstrated significant higher seminal ascorbic acid levels than any infertile group. Seminal plasma ascorbic acid in smokers and nonsmokers was correlated significantly with sperm concentration (r = 0.59, 0.60, P < 0.001), sperm motility (r = 0.65, 0.55, P < 0.001) and negatively with sperm abnormal forms per cent (r = -0.53, -0.50, P < 0.001). Nonsignificant correlations were elicited with semen volume (r = 0.2, 0.09) or liquefaction time (r = 0.03, 0.06). It is concluded that seminal plasma ascorbic acid decreased significantly in smokers and infertile men versus nonsmokers and fertile men, and is significantly correlated with the main sperm parameters: count, motility and normal morphology. Also, cigarette smoking is associated with reduced semen main parameters that could worsen the male fertilizing potential, especially in borderline cases.

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Smoking has a negative impact on semen variables. It is associated with increased sperm caspase-9, Smac/DIABLO and the percent of DNA fragmentation, especially in infertile heavy smokers.

The data support the concept of chemokines (RANTES) as mediators of liver cell injury in HCV infection. In addition, MDA and NO levels might be used as monitoring markers for oxidative stress in hepatitis C infection.

Chronic infection with hepatitis C virus (HCV) is associated with failures of T-cellmediated immune clearance and with abnormal B-cell growth and activation.HCV infection is characterized by a systemic oxidative stress that is most likely caused by a combination of chronic inflammation, iron overload, liver damage, and proteins encoded by HCV. Following viral infection, multiple pro-inflammatory mediators contribute to recruitment of immune cells to the liver and to the generation of an antiviral immune response. Recent publications mark chemokines and their receptors as key players in leukocyte recirculation through the inflamed liver. The present study involved 75 male subjects, included into two groups: Group1 (n=30) control group; group II (n=45) patients with chronic HCV. For all subjects the following investigations were performed: estimation of the levels of bilirubin, albumin, prothrombin concentration, glycosylated hemoglobin (HbA 1C), creatinine, αfetoprotein (AFP), HCV RNA, and activities of alanine and aspartate transaminases (ALT& AST) as well as alkaline phosphatase. Also, Regulated on Activation Normal T Cell Expressed and Secreted (RANTES), tumor necrosis factor alpha (TNF-α), malondialdehyde (MDA) and nitric oxide (NO) were assessed. Plasma HCV-RNA concentration (viral load) was determined by real time PCR step one using Applied Biosystem. Complete blood picture was assayed using Abbott cell dyn 3700 hematology analyzer. There were significant increase of the levels of RANTES,TNFα, MDA and NO in HCV infected patients compared with control group (P <0.05) and in these patients, these levels showed significant positive correlation with the HCV RNA viral load. Also, mild leucopenia, thrombocytopenia, neutropenia, lymphocytosis, with consequent significant increase in the lymphocytes / neutrophils (L/N) ratio were detected in these patients. Conclusion: The data support the concept of chemokines (RANTES) as mediators of liver cell injury in hepatitis C infection. In addition, MDA and NO levels might be used as monitoring markers for oxidative stress in hepatitis C infection.