Detrimental Effect Of Cigarette Smoking Research Articles

Evaluation of Effect of Cigarette Smoking on Vital Seminal Parameters which Influence Fertility.

Cigarette smoke contains many compounds which are proven carcinogens having detrimental effect on various organs. The free radicals and other carcinogens have a harmful effect on testicular function which may affect male fertility directly. Although many studies have been conducted to establish the relationship between cigarette smoking and male infertility, their conclusions have been highly controversial. This evoked our interest to investigate this intriguing research question. One hundred and twenty three subjects were included in the present study amongst which 20 were non smokers, 42 with smoking history of less than 5 years and 61 with more than 5 years. Cigarette smoking was found to have a detrimental effect on both the sperm motility and the sperm count, but the effect on sperm motility was greater than that of sperm count. This study throws light on the detrimental effect of cigarette smoking on male fertility as reflected by decreased vital parameters of semen like sperm motility and sperm count.

Through the smoke: Use of in vivo and in vitro cigarette smoking models to elucidate its effect on female fertility

A finite number of oocytes are established within the mammalian ovary prior to birth to form a precious ovarian reserve. Damage to this limited pool of gametes by environmental factors such as cigarette smoke and its constituents therefore represents a significant risk to a woman's reproductive capacity. Although evidence from human studies to date implicates a detrimental effect of cigarette smoking on female fertility, these retrospective studies are limited and present conflicting results. In an effort to more clearly understand the effect of cigarette smoke, and its chemical constituents, on female fertility, a variety of in vivo and in vitro animal models have been developed. This article represents a systematic review of the literature regarding four of experimental model types: 1) direct exposure of ovarian cells and follicles to smoking constituents’ in vitro, 2) direct exposure of whole ovarian tissue with smoking constituents in vitro, 3) whole body exposure of animals to smoking constituents and 4) whole body exposure of animals to cigarette smoke. We summarise key findings and highlight the strengths and weaknesses of each model system, and link these to the molecular mechanisms identified in smoke-induced fertility changes.

Increased activation of blood neutrophils after cigarette smoking in young individuals susceptible to COPD

BackgroundCigarette smoking is the most important risk factor for Chronic Obstructive Pulmonary Disease (COPD). Only a subgroup of smokers develops COPD and it is unclear why these individuals are more susceptible to the detrimental effects of cigarette smoking. The risk to develop COPD is known to be higher in individuals with familial aggregation of COPD. This study aimed to investigate if acute systemic and local immune responses to cigarette smoke differentiate between individuals susceptible or non-susceptible to develop COPD, both at young (18-40 years) and old (40-75 years) age.MethodsAll participants smoked three cigarettes in one hour. Changes in inflammatory markers in peripheral blood (at 0 and 3 hours) and in bronchial biopsies (at 0 and 24 hours) were investigated. Acute effects of smoking were analyzed within and between susceptible and non-susceptible individuals, and by multiple regression analysis.ResultsYoung susceptible individuals showed significantly higher increases in the expression of FcγRII (CD32) in its active forms (A17 and A27) on neutrophils after smoking (p = 0.016 and 0.028 respectively), independently of age, smoking status and expression of the respective markers at baseline. Smoking had no significant effect on mediators in blood or inflammatory cell counts in bronchial biopsies. In the old group, acute effects of smoking were comparable between healthy controls and COPD patients.ConclusionsWe show for the first time that COPD susceptibility at young age associates with an increased systemic innate immune response to cigarette smoking. This suggests a role of systemic inflammation in the early induction phase of COPD.Trial registrationClinicaltrials.gov: NCT00807469Electronic supplementary materialThe online version of this article (doi:10.1186/s12931-014-0121-2) contains supplementary material, which is available to authorized users.

Nicotine and Gastrointestinal Disorders: Its Role in Ulceration and Cancer Development

Cigarette smoke has always been the single most preventive cause of death in the world. In 2011, over 460,000 died from cigarette smoke-related diseases in US. The detrimental effects of cigarette smoke on human beings are due to the presence of many carcinogens and other components (e.g. nicotine and tar). Nicotine is now accepted as one of the major components responsible for gastrointestinal disorders. Cigarette smoking, nicotine and a nicotine-derived nitrosamine, 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) are considered as risk factors for gastrointestinal cancer, however, the underlying mechanism remains largely unknown. Previous studies reported that cigarette smoke and nicotine aggravated inflammation not only in the stomach, but also in the colon. The carcinogenic actions of cigarette smoke, nicotine and NNK on gastrointestinal cancers development have been widely studied. The strong association of cyclooxygenase-2 (COX-2) with gastrointestinal diseases has been extensively studied, however, due to the unresolved cardiovascular risk, it is of great importance to develop other new anti-cancer drugs for the treatment of cancers. This current review aims to provide an overview of the effects of cigarette smoke, nicotine and NNK on gastrointestinal inflammation, and also the carcinogenic properties in cancer development (tumor growth, angiogenesis and epithelial-mesenchymal transition). In addition, current studies on nicotinic acetylcholine receptors, adrenergic receptors and miRNAs in nicotine-related cancer pathogenesis are also highlighted.

Acute cigarette smoke exposure impairs proteasome function in the lung

Cigarette smoke mediates DNA damage, lipid peroxidation, and modification and misfolding of proteins, thereby inducing severe cellular damage. The ubiquitin proteasome system serves as the major disposal system for modified and misfolded proteins and is thus essential for proper cellular function. Its role in cigarette smoke-induced cell damage, however, is largely unknown. We hypothesized that the ubiquitin-proteasome system is involved in the degradation of cigarette smoke-damaged proteins and that cigarette smoke exposure impairs the proteasome itself. Here, we show that treatment of human alveolar epithelial cells with cigarette smoke extract (CSE) induced time- and dose-dependent cell death, a rise in intracellular reactive oxygen species, and increased levels of carbonylated and polyubiquitinated proteins. While high doses of CSE severely impaired all three proteasomal activities, low CSE concentrations significantly inhibited only the trypsin-like activity of the proteasome in alveolar and bronchial epithelial cells. Moreover, acute exposure of mice to cigarette smoke significantly impaired the trypsin-like activity by 25% in the lungs. Reduced proteasome activity was not due to transcriptional regulation of the proteasome. Notably, cigarette smoke exposure induced accumulation of polyubiquitinated proteins in the soluble and insoluble protein fraction of the lung. We show for the first time that acute exposure to cigarette smoke directly impairs proteasome activity in the lungs of mice and in human epithelial cells at low doses without affecting proteasome expression. Our results indicate that defective proteasomal protein quality control may exacerbate the detrimental effects of cigarette smoke in the lung.

The pathobiological impact of cigarette smoke on pancreatic cancer development (Review)

Despite extensive efforts, pancreatic cancer remains incurable. Most risk factors, such as genetic disposition, metabolic diseases or chronic pancreatitis cannot be influenced. By contrast, cigarette smoking, an important risk factor for pancreatic cancer, can be controlled. Despite the epidemiological evidence of the detrimental effects of cigarette smoking with regard to pancreatic cancer development and its unique property of being influenceable, our understanding of cigarette smoke-induced pancreatic carcinogenesis is limited. Current data on cigarette smoke-induced pancreatic carcinogenesis indicate multifactorial events that are triggered by nicotine, which is the major pharmacologically active constituent of tobacco smoke. In addition to nicotine, a vast number of carcinogens have the potential to reach the pancreatic gland, where they are metabolized, in some instances to even more toxic compounds. These metabolic events are not restricted to pancreatic ductal cells. Several studies show that acinar cells are also greatly affected. Furthermore, pancreatic cancer progenitor cells do not only derive from the ductal epithelial lineage, but also from acinar cells. This sheds new light on cigarette smoke-induced acinar cell damage. On this background, our objective is to outline a multifactorial model of tobacco smoke-induced pancreatic carcinogenesis.

Smoking and Soft-Tissue Dermal Fillers: A Potentially Detrimental Combination?

Sir: We read with great interest the report by Rohrich et al. regarding complications when using soft-tissue fillers.1 Given the enormous increase in the use of soft-tissue filler injections, the complication rate is likely to increase. Besides biofilms, which are comprehensively addressed in Rohrich et al.'s stimulating special topic report, we believe that other patient-related risk factors should be highlighted in this regard as well. Dr. Rees and colleagues have reported in the Journal the detrimental effect of cigarette smoking on skin flap survival in the face lift patient.2 They reported on 1186 face lift procedures performed between 1975 and 1981, with a 10.2 percent total complication rate. Active smokers had a 12.5-fold increased risk for skin flap complications compared with nonsmokers. Notably, active smoking for more than 10 years leads to facial aging by 2.5 years, according to a comprehensive twin study from the Twins Day Festival in Twinsburg, Ohio, published in the Journal in 2009.3 In May of 2008, the Journal again reported four late infections after New-Fill injections in the cheek and lips in four female patients aged 48 years.4 All suffered late infections 2 to 6 months after filler injection, and all four women were active smokers. Notably, a recent case series with three female patients with alar necrosis following dermal filler injection did not comment on any smoking history that might have interfered with an altered nasal perfusion.5 Therefore, we would suggest physicians evaluate the smoking status of a given cosmetic customer before performing soft-tissue filler injections and, when in doubt, perform quantitative cotinine assays to estimate the risk for potential malperfusion. This is especially important among patients who have had previous surgical interventions, such as rhinoplasty or face lifts, with potentially altered vasculature. Karsten Knobloch, M.D. Peter M. Vogt, M.D., Ph.D. Plastic, Hand, and Reconstructive Surgery Hannover Medical School Hannover, Germany

Natural Killer Cells in Obesity: Impaired Function and Increased Susceptibility to the Effects of Cigarette Smoke

BackgroundObese individuals who smoke have a 14 year reduction in life expectancy. Both obesity and smoking are independantly associated with increased risk of malignancy. Natural killer cells (NK) are critical mediators of anti-tumour immunity and are compromised in obese patients and smokers. We examined whether NK cell function was differentially affected by cigarette smoke in obese and lean subjects.Methodology and Principal FindingsClinical data and blood were collected from 40 severely obese subjects (BMI>40 kg/m2) and 20 lean healthy subjects. NK cell levels and function were assessed using flow cytometry and cytotoxicity assays. The effect of cigarette smoke on NK cell ability to kill K562 tumour cells was assessed in the presence or absence of the adipokines leptin and adiponectin. NK cell levels were significantly decreased in obese subjects compared to lean controls (7.6 vs 16.6%, p = 0.0008). NK function was also significantly compromised in obese patients (30% +/− 13% vs 42% +/−12%, p = 0.04). Cigarette smoke inhibited NK cell ability to kill tumour cell lines (p<0.0001). NK cells from obese subjects were even more susceptible to the inhibitory effects of smoke compared to lean subjects (33% vs 28%, p = 0.01). Cigarette smoke prevented NK cell activation, as well as perforin and interferon-gamma secretion upon tumour challenge. Adiponectin but not leptin partially reversed the effects of smoke on NK cell function in both obese (p = 0.002) and lean controls (p = 0.01).Conclusions/SignificanceObese subjects have impaired NK cell activity that is more susceptible to the detrimental effects of cigarette smoke compared to lean subjects. This may play a role in the increase of cancer and infection seen in this population. Adiponectin is capable of restoring NK cell activity and may have therapeutic potential for immunity in obese subjects and smokers.

Retrospective Assessment of Potential Negative Synergistic Effects of Varicocele and Tobacco Use on Ultrastructural Sperm Morphology

To investigate, in a retrospective study, whether smoking cigarettes increases the effect of varicocele on sperm morphology. The semen quality of 2 groups of patients with varicocele were compared, those who smoked (n = 121) and those who did not (n = 158). The semen parameters were evaluated, and sperm morphology was assessed using transmission electron microscopy and quantitatively elaborated (fertility index, immaturity, necrosis, and apoptosis percentages). In the smoker and nonsmoker varicocele-associated cases, sperm motility and the results from transmission electron microscopy analysis were significantly impaired compared with controls. However, a nonsignificant difference was detected when the semen parameters were compared. Subsequently, we divided the patients into 4 groups: mild (> or = 1 but < or = 10 cigarettes/d), moderate (>10 but <20 cigarettes/d), and heavy (> or = 20 cigarettes/d) smokers and a group of randomly chosen nonsmoker patients with varicocele. The sperm motility, sperm concentration, and fertility index decreased and the percentage of sperm pathologic features increased as the number of cigarettes smoked daily increased. A detrimental effect of cigarette smoking (>10 cigarettes/d) associated with varicocele on sperm motility and morphology was observed. Because much of reduced fecundity associated with smoking may be reversed within 1 year of cessation, as reported in published studies, effective interventions targeted at helping patients quit smoking should be addressed for the benefit of general health and fertility.

The differential effect of cigarette smoking on glomerular filtration rate and proteinuria in an apparently healthy population

The detrimental effects of cigarette smoking on the kidney in healthy individuals without established renal diseases have not been established. We evaluated the effects of smoking on renal function and proteinuria in 35 288 apparently healthy participants who were not on antihypertensive and/or antidiabetic medication and who had undergone a health examination at the Health Promotion Center, Seoul National University Hospital from 1995 to 2006. Renal function was estimated using the simplified Modification of Diet in Renal Disease Study equation for estimated glomerular filtration rate (eGFR), and proteinuria was determined by the spot urine dipstick test. Adjusted eGFR was higher in current smokers (mean+/-s.e.m., 79.3+/-0.1 ml min(-1)) than in ex-smokers (77.3+/-0.2 ml min(-1), P<0.001) and non-smokers (77.7+/-0.1 ml min(-1), P<0.001). The adjusted eGFR of smokers who smoked >20 cigarettes per day were higher than that of individuals who smoked < or =20 cigarettes per day (P<0.001). In participants with an eGFR of <50 ml min(-1), current smoking (38.3+/-1.9 ml min(-1)) and past smoking (39.5+/-1.9 ml min(-1)) were associated with significantly lower eGFR values than non-smoking (45.1+/-1.2 ml min(-1); P=0.007 and P=0.027, respectively). Current smoking was associated with a higher risk of proteinuria (urine dipstick for albuminuria > or =1+) than non-smoking (odds ratio=1.380, P<0.001). In conclusion, cigarette smoking is associated with a higher eGFR in the general population, whereas it might reduce eGFR in a small subset of the population and increase the risk of proteinuria. These subsets should be better defined to prevent chronic kidney diseases related to smoking in the general population.

Genetic Ablation of NADPH Oxidase Enhances Susceptibility to Cigarette Smoke-Induced Lung Inflammation and Emphysema in Mice

Cigarette smoke (CS) induces recruitment of inflammatory cells in the lungs leading to the generation of reactive oxygen species (ROS), which are involved in lung inflammation and injury. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is a multimeric system that is responsible for ROS production in mammalian cells. We hypothesized that NADPH oxidase-derived ROS play an important role in lung inflammation and injury and that targeted ablation of components of NADPH oxidase (p47(phox) and gp91(phox)) would protect lungs against the detrimental effects of CS. To test this hypothesis, we exposed p47(phox-/-) and gp91(phox-/-) mice to CS and examined inflammatory response and injury in the lung. Surprisingly, although CS-induced ROS production was decreased in the lungs of p47(phox-/-) and gp91(phox-/-) mice compared with wild-type mice, the inflammatory response was significantly increased and was accompanied by development of distal airspace enlargement and alveolar destruction. This pathological abnormality was associated with enhanced activation of the TLR4-nuclear factor-kappaB pathway in response to CS exposure in p47(phox-/-) and gp91(phox-/-) mice. This phenomenon was confirmed by in vitro studies in which treatment of peritoneal macrophages with a nuclear factor-kappaB inhibitor reversed the CS-induced release of proinflammatory mediators. Thus, these data suggest that genetic ablation of components of NADPH oxidase enhances susceptibility to the proinflammatory effects of CS leading to airspace enlargement and alveolar damage.

Effects of Pre- and Post-natal smoke exposure on airway neural responses

AbstractAbundant epidemiological data shows that maternal smoking during pregnancy or second-hand smoke exposure during neonatal life and infancy increases the incidence of respiratory illnesses later in life. However, underlying mechanisms initiated in early life but affecting adult disease remain undefined. Neurotrophins, including nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), are neurotrophic factors essential in promoting and maintaining differentiation, growth, and survival of central and peripheral nervous system. The goal of this proposal is to examine the potential role of neurotrophin release in mediating long-term effects of prenatal and early postnatal smoke exposure. Our studies showed that an initial exposure to smoke during prenatal and early postnatal periods significantly changed lung function, substance P (SP) innervation in trachea and the level of NGF in BAL fluid after re-exposure to smoke on adult (postnatal day (PD) 60). In controls, smoke exposure (PD 28) with a subsequent re-exposure at PD 60 did not affect lung function or SP innervation or NGF levels. PCR array revealed enhanced expression of multiple genes including NGF and its receptor by smoke exposure only during early prenatal periods. These data suggest that a critical period of exposure exists in early periods of development. Increased expression of NGF and its receptor in airway caused by smoke exposure may enhance susceptibility to respiratory illnesses in adult. These findings have obvious and significant implication both for smoking during pregnancy and the effects of second hand tobacco smoke exposure. The study provides evidence that prenatal and early postnatal life are periods of enhanced susceptibility to detrimental effects of cigarette smoke. These effects appear to be mediated through the release of neurotrophic factors like NGF which regulate growth and maturation of the airway during these susceptible periods.

Cigarette Smoking and Adenomatous Polyps: A Meta-analysis

Through the past 2 decades, a consistent association between cigarette smoking and colorectal adenomatous polyps, recognized precursor lesions of colorectal cancer, has been shown. We performed a meta-analysis to provide a quantitative pooled risk estimate of the association, focusing on the different characteristics of the study populations, study designs, and clinical feature of the polyps. We performed a comprehensive literature search of studies linking cigarette smoking and adenomas. We used random effects models to evaluate pooled relative risks and performed dose-response, heterogeneity, publication bias, and sensitivity analyses. Forty-two independent observational studies were included in the analysis. The pooled risk estimates for current, former, and ever smokers in comparison with never smokers were 2.14 (95% confidence interval [CI], 1.86-2.46), 1.47 (95% CI, 1.29-1.67), and 1.82 (95% CI, 1.65-2.00), respectively. The association was stronger for high-risk adenomas than for low-risk adenomas. Studies in which all controls underwent full colonoscopy showed a higher risk compared with studies in which some or all controls underwent partial colon examination. This meta-analysis provides strong evidence of the detrimental effect of cigarette smoking on the development of adenomatous polyps. Smoking is important for both formation and aggressiveness of adenomas.

'New Parenting', Psychotherapy, Prenatal and Perinatal Care

The health of future generations, both physical and psychological, depends upon good parental and early environment, free particularly from malnutrition, toxins and undue stress. Education about these negative influences is urgent, especially to encourage childbearing women in a healthy diet and lifestyle. The detrimental effects of cigarette smoking in pregnancy have been known since the 1970s, yet in Germany, for example, 60% of all children are conceived, carried, born into a household where at least one adult smokes. Even if the father desists from smoking at home, the nicotine in his body tissues is transmitted to anyone near him, for example his wife when they sleep near each other. More than one glass of beer, wine or spirits per week during the pregnancy can be detected at birth. Alcohol in early in the pregnancy--just when many mothers are unaware they are pregnant--an produce significant physical malformation, especially in the face. Prenatal exposure to alcohol has signilfcant effects on the intelligence and behaviour of the child. Many of these children are very restless. Even slight amounts of poisoning during the pregnancy are related to the development of a negative self-image and the compensatory behaviour of the Narcissistic Personality Disorder in later life. The Prenatal Deprivation and Poisoning Syndromes have not only been related to heart disease and eating disorders in the area of general health but also in the area of psychological health to the Borderline Personality Disorder. Undue stress of any kind during the pregnancy leads to problems for the developing child.

Follicle growth is inhibited by benzo-[a]-pyrene, at concentrations representative of human exposure, in an isolated rat follicle culture assay

The adverse effects of cigarette smoking on human fertility have been well documented. However, the mechanism(s) underlying the detrimental effects of cigarette smoking are unknown. Using a novel isolated rat follicle culture assay, we tested the hypothesis that benzo-[a]-pyrene (B[a]P), a constituent of cigarette smoke, can inhibit follicle growth. B[a]P levels were quantified in the serum and follicular fluid (FF) of women undergoing in vitro fertilization (IVF) treatment exposed to mainstream smoke (n = 19) and non-smokers (n = 10) by gas chromatography mass spectrometry. Isolated rat follicles were cultured with increasing concentrations of B[a]P (1.5-300 ng ml(-1)) and follicle diameter was measured daily. Mean ( +/- Standard error of the mean) B[a]P) was quantified in the serum (0.40 +/- 0.13 ng ml(-1)) and FF (1.32 +/- 0.68 ng ml(-1)) of women who smoke. IVF stimulation and outcome measures were similar between female smokers and non-smokers with the exception of implantation rate and pregnancy rate, which were both significantly lower (P < 0.05) in the MS group. B[a]P treatment significantly reduced rat follicle diameter and attenuated FSH stimulated growth in a dose-dependent manner, beginning at 1.5 ng ml(-1). Our data suggest that B[a]P, at levels representative of those measured in human FF, may adversely affect follicle development and be an ovarian toxicant.

Commentary: Smoking and atherosclerotic diseases in Asia—the implication in global atherosclerosis prevention

that smoking is a risk factor for both coronary heart disease (CHD) and stroke, independent of the effects of BMI, blood pressure, and cholesterol, with the amelioration of the effects after quitting. Of much interest and importance, Asians and Caucasians (in Australia and New Zealand) had similar increased proportional cardiovascular risk (relative risk) from smoking cigarettes, and similar relative risk reduction from quitting. Moreover young people and women had greater relative risk of cardiovascular disease from smoking, but the effect declined with age. This report also appropriately documented relative and attributable risks for CHD and strokes in different groups. While there were no differences in their relative risk, the attributable risk for CHD from smoking reflected the prevalence of smoking in different groups and, hence, was higher in Chinese men (30%) compared with Australian (13%) and New Zealand men (7%) but was lower in Chinese women (3%) compared with the other two groups (11% for Australia and 6% for New Zealand). However, it should be noted that the overall absolute risk of CAD (fatal and non-fatal) in Australia and New Zealand (2.6%) is still higher than that in Asia (0.35%), possibly reflecting the effects of different genes and gene‐environment interactions in the two regions. Time will tell whether these differences in absolute risk will converge and abolish, with the changing trend of smoking and modernization in the two regions. The greater smoke-related impact on cardiovascular health of young women is of much public health concern, given that the tobacco epidemic is still spreading among women (estimated 530 million by 2025) and that, although prevalence rates are low in Asian women, the high rates in men mean that they are exposed to high levels of passive smoking. Tobacco control policies should, therefore, always include messages specifically targeted at women. The strength of this paper is its large sample size. However, it is important to note that the present study is a retrospective overview ‘meta-analysis’ of 40 observational studies spreading over 37 years from 1961 to 1998, using non-uniform study protocols and data entries for smoking status and smoking (inhalation) habits. The types of cigarette smoked, changes in inhalation habits overtime and years of follow-up were not uniformly available. In addition, information on many important confounding factors, including body mass index, blood pressure, and cholesterol levels were missing in some of these cohorts, and the cholesterol assay understandably were carried out in different laboratories, using different methods and standardization, over a long period of 37 years. It may be quite Atherosclerotic disease including stroke and coronary artery disease (CAD) is the most important health issue of modern society. Cigarette smoking has been associated with this disease in Western countries. 1 In comparison, the impact of smoking on cardiovascular health has been less well documented in Asia, and, in particular, its impact in China where the population at risk currently comes up to one-quarter of the global population is unclear. Interest in the impact of smoking in China is inspired by the fact that although 70% of Chinese males smoke (compared with current prevalence in the range 20‐30% for men in most Western populations), the prevalence of CAD in Chinese men is one-quarter of that for Western men. 2 Furthermore, there is evidence that young Chinese adults have less arterial endothelial dysfunction (a novel surrogate atherosclerosis marker predictive of cardiovascular outcome) than white adults with similar direct or indirect exposure to cigarette smoke. 3 A second cross-sectional study, similarly using a surrogate marker of cardiovascular disease [carotid intimamedia thickness (IMT)], found that Chinese adults who had Western lifestyles had thicker IMT than native rural Chinese, and that the detrimental effect of cigarette smoking on IMT was greater in Westernized Chinese living in Hong Kong and Sydney than it was in native rural Chinese. 4 These differences suggest a relative protection of Chinese from the effect of cigarette smoking, possibly due to certain gene differences, which may be modified by Westernization, and subscribe to a gene‐ environment interaction process, or to an interaction between smoking, changes in lifestyles, and other risk factors in the process of Westernization. While evaluation of the underlying lifestyles, dietary habits, and subsequently physiological and biochemical changes related to such Westernization process are awaited with much interest, these early results call for further studies that examine and compare smoking-related effects in acculturated migrant Chinese population with those in village natives in mainland China. 5 To illuminate this important health issue, the paper from the Asian Pacific Cohort Studies Collaboration in this issue of the journal 6 addressed the problem from an epidemiological perspective. With the strength of large numbers of subjects (n = 562 338) and, therefore, more precise estimates, they confirmed

1516: Relationship between Cigarette Smoking and the Levels of Antioxidants and Leukocytes in Infertile Men: A Prospective Study

Introduction and Objective: Cigarette smoke is a known somatic cell mutagen and carcinogen and it is known to adversely affect male reproductive health. Even though studies have shown the harmful effets of smoking on sperm quality, a handful of studies have found no association between smoking and sperm function or sperm nuclear DNA damage. Superoxide dismutase (SOD) and catalase are important antioxidant enzymes that can quench excess free radicals such as: superoxide anion and hydrogen peroxide respectively. The objective of our study was to evaluate and correlate the seminal antioxidant enzymatic activity (SOD and catalase levels) among fertile and infertile men who are cigarette smokers. Methods: The Institutional Review Board approved this study. Ten fertile donors and 112 infertile patients were included in the study. Semen analysis was performed according to the World Health Organization guidelines and sperm morphology according to Kruger strict criteria. Superoxide dismutase and catalase levels were determined with a spectrophotometer. Results: A significant difference was noted in the number of cigarettes smoked/day between infertile (4.8 ± 0.9) and fertile men (1.5 ± 0.5; p = 0.03). Significantly lower levels of SOD (14.67 ± 12.27 and 38.03 ±21.65) and catalase (14.87 ± 16.95 and 34.03 ± 20.65) were seen in infertile patients compared to fertile donors (P <0.0001). A significant correlation between catalase and SOD was observed (r = 0.461, P = 0.0001). Superoxide dismutase was significantly correlated with sperm concentration (r = 0.204, P = 0.034) and negatively correlated with leukocytospermia (r = -0.228, P = 0.021). Cigarette smoking was inversely correlated with SOD levels (r = -0.251, P = 0.01), but not with catalase levels (r = -0.147, P = 0.130). Conclusions: Decreased antioxidant enzyme levels are associated with male infertility. The detrimental effects of cigarette smoking on sperm motility and antioxidant levels (negative correlation with SOD) may be a possible reason for infertility in men who smoke cigarettes. As low antioxidant levels are linked to decreased fertility, physicians should advise infertile patients who smoke cigarettes to quit smoking. Author Disclosure Block: E.B. Pasqualotto, None; F.M. Umezu, None; A. Agarwal, None; M. Salvador, None; F.F. Pasqualotto, None.

Aberrant antibody responses to oxidized LDL and increased intimal thickening in apoE−/− mice exposed to cigarette smoke

Cigarette smoking is associated with increased atherosclerosis and intimal thickening, and has immune-suppressive effects. The immune system modulates atherosclerosis and intimal thickening. We hypothesized that detrimental effects of cigarette smoke (CS) involves modulation of the immune response to oxidized low-density lipoprotein (oxLDL). ApoE−/− mice fed Western diet were exposed to CS starting at 20 weeks of age. Control mice were exposed to air. After 5 weeks of CS, mice were subjected to carotid arterial cuffing for 21 days. Intimal thickening was significantly increased in CS mice compared to control (0.050±0.034 mm 2 versus 0.023±0.021 mm 2; P<0.05). Spleen lymphocyte population, cytokine mRNA expression, and total IgM and IgG levels were similar. Anti-MDA oxLDL IgG was reduced by 40% ( P<0.05) in CS mice compared to control. Copper-oxidized LDL IgG antibodies remained unchanged but IgM increased in CS mice, associated with increased intimal thickening. Anti-phosphorylcholine (PC) IgM was also increased in the CS mice, associated with increased intimal thickening. Lymphocyte signaling molecule lymphotoxin β (LTβ) expression was significantly decreased in spleens of CS exposed mice. Our results suggest that immune modulation by CS characterized by aberrant antibody responses to oxLDL and reduced LTβ mRNA expression is associated with increased intimal thickening after arterial cuffing.

1420: Detrimental Effect of Cigarette Smoking on Erectile Dysfunction in the Rat is Contingent to Diabetes as Co-Morbidity

You have accessJournal of UrologyDiscussed Poster, Tuesday, May 11, 2004, 8:00 am - 12:00 pm1 Apr 20041420: Detrimental Effect of Cigarette Smoking on Erectile Dysfunction in the Rat is Contingent to Diabetes as Co-Morbidity Hugo H. Davila, Monica G. Ferrini, Thomas R. Magee, Jacob Rajfer, and Nestor F. Gonzalez-Cadavid Hugo H. DavilaHugo H. Davila More articles by this author , Monica G. FerriniMonica G. Ferrini More articles by this author , Thomas R. MageeThomas R. Magee More articles by this author , Jacob RajferJacob Rajfer More articles by this author , and Nestor F. Gonzalez-CadavidNestor F. Gonzalez-Cadavid More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(18)38645-2AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "1420: Detrimental Effect of Cigarette Smoking on Erectile Dysfunction in the Rat is Contingent to Diabetes as Co-Morbidity." The Journal of Urology, 171(4S), p. 374 © 2016 by American Urological AssociationFiguresReferencesRelatedDetails Volume 171Issue 4SApril 2004Page: 374 Advertisement Copyright & Permissions© 2016 by American Urological AssociationMetricsAuthor Information Hugo H. Davila More articles by this author Monica G. Ferrini More articles by this author Thomas R. Magee More articles by this author Jacob Rajfer More articles by this author Nestor F. Gonzalez-Cadavid More articles by this author Expand All Advertisement PDF downloadLoading ...

Cigarette smoking damages women's reproductive life

Female smokers experienced menopause significantly ( P ≤ 0.000001) earlier than non-smokers (47.1 ± 3.3 versus 49.4 ± 3.6 years, mean age at menopause ± SD) and the prevalence of cigarette smoking is more frequent in females with ovarian failure before 46 years of age. These data are consistent with a possible detrimental effect of cigarette smoking on ovarian function and suggest new investigations are needed in this field. Detailed information about this important negative effect is strongly recommended, particularly for female smokers of reproductive age.