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Chen Runqiang Mo Jianfeng

(Department of Urology, Qingyuan People's Hospital)

The influence of smoking on male reproductive system lies in that its smoke contains many chemical carcinogens and carcinogen precursors, which affects the quality of male semen, damages testis and epididymis, and affects sex hormones and sexual function.

Keywords smoking; Male; breed

Smoking, people often only think about affecting lung health. As we all know, cigarette smoke contains a variety of chemical carcinogens and carcinogen precursors, which has been recognized as one of the main risk factors of many diseases and tumors, and has been widely confirmed in epidemiology, cytogenetics and molecular genetics. A lot of research has been done at home and abroad on the influence of smoking on reproductive function. This paper reviews the effects of smoking on male semen quality, testicular and epididymal damage, sex hormones and sexual function and its possible mechanism.

1. Effect of smoking on male semen quality

Semen quality is usually measured by various indicators, such as semen volume, semen pH value, sperm density, sperm quantity, percentage of sperm moving forward, sperm survival rate and percentage of normal sperm morphology. Kunzle et al. studied smoking and semen quality in infertile people. The results showed that the sperm density and normal sperm rate of smokers were significantly lower than those of non-smokers. Kunzle et al. studied 655 infertile men who smoked and 1 13 1 non-smoking, and found that compared with non-smokers, the sperm density, the total sperm count and the number of sports sperm of smokers decreased significantly, by 15.3%, 17.5% and respectively. The normal sperm rate of smokers was 265,438 0.2%, which was lower than that of non-smokers (23.7%) (P=0.0007). However, the sperm survival rate, semen volume and fructose concentration of smokers also decreased slightly, but they did not reach the statistically significant level. Vine metallic aluminum. More than 20 papers were meta-analyzed. The results showed that compared with non-smokers, the sperm density of smokers decreased by 13%- 17%, but no obvious dose-effect relationship was found, while the sperm motility decreased by about 20%. Zhang Aiying and others randomly selected 1 10 smokers and1/kloc-0 non-smokers consulted before pregnancy as the research objects. The subjects were 23-36 years old and had normal health in the past, excluding oligozoospermia and azoospermia. The smoking period in the smoking group is 2- 15 years, and the smoking amount is 3-30 cigarettes/d; The non-smoking group never smokes. The results of semen examination showed that the sperm rate of normal morphology and rapid forward movement in smoking group was significantly lower than that in non-smoking group, and the sperm survival rate was slightly lower than that in non-smoking group. There was no significant difference in semen volume and sperm density between smoking group and non-smoking group. Guan Zhibao also found that there were significant differences in sperm survival rate and sperm density between smoking group and non-smoking group (P

2. Testicular and epididymal injuries

In smoking rats, leydig cells and germ cells decreased and sertoli cells were damaged. The ultrastructure of testis showed a series of changes: the collagen fibers in the basal layer increased, the intrinsic membrane thickened, and the contractile cells around the tube separated. The tight junction between sertoli cells is weakened, the mitochondria are diverse in morphology, accompanied by the increase of irregular ridges and high electron density matrix, the accumulation of intracellular lipid droplets and the formation of multinuclei. Smoker testicular atrophy, spermatogenesis decreases and stops. In normal male smokers, the concentration of α -glucosidase secreted by epididymis decreased significantly, which indirectly proved the harmful effects of smoking on epididymis. This damage affects the maturation of sperm in epididymis, leading to the decline of sperm vitality and insemination ability. Animal experiments have confirmed that cadmium is a toxic substance that directly causes testicular damage. The cadmium concentration in the testis of smoking rats is higher than that of the control group, which leads to testicular damage, blood-testis barrier destruction and spermatogonia destruction in seminiferous tubules, which affects the normal spermatogenic function. The arrangement of epididymal duct epithelium is disordered, large vacuoles appear, the blood-epididymal barrier is destroyed, and the damaged sperm passes through epididymal duct, which is also the main cause of spermatogenesis disorder. Similarly, the cadmium concentration in the seminal plasma of smokers also increased significantly.

2. Effect on sex hormones

Sofikitis et al found that there was no significant difference in the levels of testosterone (T), luteinizing hormone (LH) and follicle stimulating hormone (FSH) in peripheral blood between normal male smokers and non-smokers. There was no significant difference in serum T between smoking group and non-smoking group, but the serum T level in smoking group decreased significantly after gonadotropin stimulation. Other studies have different results: the serum levels of total T, free T, T and LH of smokers are significantly increased, but the levels of bioavailable T and 17-β estradiol (E2) are not different. The increase of LH in smokers explains the stimulation of pituitary gland to interstitial cells and the increase of T, but the increase of androgen binding protein suggests that the increase of serum total T and free T levels is due to the change of plasma androgen binding protein, not the influence of smoking. In a group of long-term heavy smokers, the serum T value decreased obviously, suggesting that under the long-term influence and inhibition of harmful substances from cigarettes, the ability of testicular interstitial cells to synthesize T also decreased. In the above research, the contradictory result of constant, increasing and decreasing T level may be because smoking can affect male reproductive endocrine system in many ways. The difference of measured values in some studies may be related to the amount and duration of inhaled smoke. In the early stage of smoking, T secretion can be promoted by stimulating interstitial cells. With the extension of smoking time, the function of interstitial cells decreased and T production decreased. However, what substances in cigarette smoke will damage the reproductive system, what is the relationship between cigarette varieties and reproductive system damage, and what links affect the hypothalamus-pituitary-testis axis need further study.

4. Influence on sexual function

Smoking can lead to changes in penile hemodynamics, penile vascular sclerosis, thrombosis, and changes in penile cavernous blood flow, affecting penile erectile function and further aggravating male erectile dysfunction. Under electron microscope, it can be observed that the cavernous vascular wall of male smoking rats is thickened and there are particles accumulation in the intima of blood vessels. Rats did not ride or observe penis congestion, which confirmed that smoking caused sexual dysfunction in rats. Although the influence of smoking on male reproduction is controversial, some studies have pointed out that men can improve sperm density, vitality and sperm movement function after quitting smoking.

5. Possible mechanisms

Cigarettes contain a lot of harmful substances, such as nicotine, conidine, benzo -a- pyrene, carbon monoxide (CO), cadmium (Cd), lead (Pb) and other heavy metals, which have adverse effects on male reproductive function. There are many possible mechanisms, and some specific mechanisms are still under study. Zhou Xinglin's research on rats shows that after long-term heavy smoking, many harmful substances in cigarettes will gradually accumulate in rats, which will interfere with the microcirculation of testis and the exchange of substances with the environment, thus leading to testicular edema, congestion, degeneration and necrosis, the disintegration of mitochondria of testicular spermatogonia, the decrease of spermatogenic cells at all levels of seminiferous tubules, the shedding of spermatogenic skin and the deformity or loss of sperm in the cavity. In addition, the harm of smoking to male reproduction also involves cadmium and nicotine in tobacco. Nicotine can affect the germ cells of male testis, inhibit the secretion of sex hormones and kill sperm, resulting in a decrease in sperm count. Cd entering the body is easy to accumulate in testicular tissue. Excessive intake of cadmium can lead to obvious histopathological changes in testicular tissue. At the same time of testicular tissue injury, the levels of androgen and gonadotropin in blood also changed. Xu et al. studied 22 1 Singaporean men, and found that the blood cadmium content in patients with semen deficiency and oligozoospermia was negatively correlated with sperm density (r=-0.24, P < 0.05), and the cadmium content in semen was negatively correlated with sperm output (r=-0.24, P