Cigarette Smoking

Tobacco plants, like many other plants, will invariably contain certain amounts of lead absorbed from the soil; however, lead may also be deposited on the surface of the leaves. The widespread use of lead arsenate as a pesticide on tobacco crops has, in the past, resulted in lead contamination of tobacco products. The effect of tobacco constituents on classical sperm parameters and fertility has been under investigation for decades [47].

Kunzle et al. [48], when evaluating many men attending a fertility clinic, found that cigarette smoking was associated with reductions in sperm concentration, motility, and normal morphology. Gaur et al. [49] showed that motility is one of the first sperm parameters affected and asthenozoospermia may be an early indicator of reduced semen quality in light smokers. They reported significantly high teratozoo-spermia in heavy smokers compared with nonsmokers.

In a study conducted on fertile men, it was observed that fertile men who were smokers showed reductions in semen volume in comparison with nonsmokers, and this reduction in semen volume was in proportion to the number of cigarettes smoked [5] .

The largest cross-sectional study, including 2,542 healthy males, on this issue was carried out and published by Ramlau-Hansen et al. [50] and it showed that with increasing smoking, a 20-30% reduction in sperm count, volume and motile spermatozoa were observed. A study on voluntary males of reproductive age showed that after ejaculation, sperm motility deteriorated much more rapidly in heavy smokers in comparison to controls [51].

However, the exact effect of smoking on male fertility remains controversial. Toxic metabolites in smoke, such as nicotine, carbon monoxide, recognized carcinogens and mutagens such as radioactive polonium, cadmium, benzo(a) pyrene, and others have been demonstrated to be negatively associated with the normal development of male and female gametes and embryos [52, 53] .

Also, direct exposure of spermatozoa to the toxins in cigarettes smoke probably tilts the delicate balance of ROS that are produced by spermatozoa for their special functions such as capacitation and acrosome reaction. Increased quantities of ROS have been shown to be detrimental to the DNA of spermatozoa, thus producing a negative effect on the viability and morphology of spermatozoa [54].

In fact, cigarette smoking has been associated with significantly increased levels of seminal ROS, which cause oxidative stress [6]. Cigarette smoking may inversely affect sperm quality and decrease the antioxidant activity in seminal plasma [7].

The exact molecular mechanisms for these effects are not well understood [55]. Animal models using rats linked the reduction of sperm developmental processes and fertility with mutagenic components of smoke [56] . These metabolites may cause deficiencies in spermatogenesis and chromatin condensation and reductions in sperm motility and the number of germ cells [57], as well as induction of apopto-sis in the genital cells of the rat testes [58], a secretory deficit ofLeydig and Sertoli cells [59], or impairment of testicular histology [60].

Different groups have studied sperm DNA fragmentation in smoking and nonsmoking men from infertile couples. An increased rate of sperm DNA fragmentation in smokers was found in pre and post-swim-up samples [61]. The protamine deposition can also be incomplete in smokers, resulting in ratios of histone to protamine and of protamine 1 to protamine 2 that differ from the normal. Both types of defects in spermiogenesis are associated with subfertility or infertility [62]. Oxidative stress occurs in seminal plasma of male smokers with increased levels of seminal ROS and with increases in the concentrations of cadmium and lead and with decreases in the concentration of ascorbic acid and the activity of other components of the antioxidant defense mechanism [6, 7] [ Infertile men who smoke have higher levels of seminal oxidative stress indicators than infertile nonsmokers [6]. Oxidative stress has been shown to be a major cause of male infertility; a large proportion of infertile men were shown in one study to have elevated levels of seminal ROS [4]. ROS causes oxidative damage to normal sperm DNA, proteins and lipids, which may be related to sperm abnormalities [1][ Moreover, plasma membranes of spermatozoa, whose physically properties and functional integrity largely determine motility and fertilizing ability, hold a large amount of polyunsaturated fatty acids, prone to oxidative injury, whereas the cytoplasm contains low concentrations of antioxidant enzymes [63],

Cotinine concentrations in seminal plasma are considered as a biomarker for smoking [64]. A significant negative correlation was detected with P2 levels in spermatozoa, and a significant positive correlation was detected with P1/P2 ratios [65]. This is the first study conducted to evaluate the effect of smoking on the protamina-tion process. It demonstrates the negative effect of smoking on protamination of sperm chromatin and indicates that the reason for higher P1/P2 ratios in smokers is the underrepresentation of P2, suggesting that smoking may affect P2 expression greater than P1. Smoking affects either the structure of protamines or their binding to DNA or affects sperm DNA directly through increasing oxidative damage.

Some investigators have described seminal leukocytes as a possible source of free radicals [66, 67]. The status of ROS-induced spermatic damage depends on the location of the inflammatory reaction, on the duration of the exposure of the sperm to these products, and the ability of the spermatic cell to activate its intrinsic defense system [68] .

Recently, a study evaluated the levels of plasma ascorbic acid levels in smokers. The study showed a significant decrease in the mean seminal plasma ascorbic acid levels in smokers vs. nonsmokers in all groups. Also, in 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, sperm motility, but negatively with sperm abnormal forms. The study concluded that seminal plasma ascorbic acid decreases significantly in smokers and infertile men vs. nonsmokers and fertile men, and correlates 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 [69].

DNA fragmentation index, high DNA stainability and round-head sperms are increased in idiopathic infertile men; this increase is associated with cigarette smoking. These defects may be attributed to increased oxidative stress and insufficient scavenging antioxidant enzymes in the seminal fluid of infertile patients [70].

The extent of these alterations was lesser in the group administered with nicotine along with selenium [71]. Analysis of plasma revealed reduced quantity of cotinine in the group coadministered with nicotine along with selenium in comparison with the nicotine group. Nondetectable levels of nicotine were present in the coadminis-tered group. This indicates altered metabolism of nicotine when administered along with selenium.

A Disquistion On The Evils Of Using Tobacco

A Disquistion On The Evils Of Using Tobacco

Among the evils which a vitiated appetite has fastened upon mankind, those that arise from the use of Tobacco hold a prominent place, and call loudly for reform. We pity the poor Chinese, who stupifies body and mind with opium, and the wretched Hindoo, who is under a similar slavery to his favorite plant, the Betel but we present the humiliating spectacle of an enlightened and christian nation, wasting annually more than twenty-five millions of dollars, and destroying the health and the lives of thousands, by a practice not at all less degrading than that of the Chinese or Hindoo.

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