Effect of nicotine on spermatogenesis in adult albino rats

Abstract

This study aimed to assess the effects of nicotine on spermatogenesis in 140 mature male albino rats divided into group A (controls), group B (sham controls), group C (nicotine treated) and group D (nicotine withdrawal). Group C was subdivided into CI, CII, CIII according to the dose of injected nicotine (0.2, 0.4 and 0.6 mg nicotine per 100 g per day), where each subgroup was further subdivided according to the treatment duration into subgroups a, b and c that received nicotine for 2, 4 and 8 weeks. Group D received nicotine for 8 weeks followed by withdrawal for another 8 weeks to assess testicular recovery. Testicular tissue sections were subjected to haematoxylin and eosin, Masson's trichrome stains and morphometry. The results showed that nicotine caused degenerative changes in the seminiferous tubules, revealed by altered general tubular architecture, decreased thickness of the spermatogenic cell masses, Sertoli cell vacuolation and thickened basal lamina. These changes were proportional to the nicotine dose and duration. Following nicotine withdrawal, regeneration of the damaged seminiferous tubules was observed to be rather complete in CI group. It is concluded that nicotine could adversely affect testicular spermatogenesis in a dose- and time-dependent manner which would be almost reversible after nicotine withdrawal, especially after small doses.

Antioxidant and anti‐apoptotic effects of royal jelly against nicotine‐induced testicular injury in mice

“…It has been reported that NIC causes Leydig cells dysfunction and decreases the testosterone level . According to relevant studies, increase in the dose of NIC leads to the reduction in germ cell proliferation . Due to the importance of Leydig cells in the secretion of testosterone, which plays the key role in spermatogenesis, destruction of these cells can be a major cause of apoptosis and cell death elevation.…”

“…Therefore, NIC causes disturbances in the functions of cells and induces oxidative stress and apoptosis through exerting effects on acetylcholine receptors. It has been shown that NIC causes damages to the reproductive system via increase in the levels of the ROS and MDA in reproductive tissues . Cotinine, a NIC metabolite, similar to NIC, enhances production of free radicals and ROS in testicular tissue and can lead to the lipid peroxidation generation ultimately inducing cellular damages …”

“…16 According to relevant studies, increase in the dose of NIC leads to the reduction in germ cell proliferation. 50 The NIC merely crosses cell membranes and interferes with proteins and cellular components within the cytoplasm of cells undergoing division. 52 The acetylcholine and NIC receptors not only are present in nerve and muscle cells, but also in the most of nonnervous cells such as cells in the reproductive system.…”

“…It has been shown that NIC causes damages to the reproductive system via increase in the levels of the ROS and MDA in reproductive tissues. 12,50,54 Cotinine, a NIC metabolite, similar to NIC, enhances production of free radicals and ROS in testicular tissue 12,55 and can lead to the lipid peroxidation generation ultimately inducing cellular damages. 56 According to previous reports, diminishing germ cell population following NIC exposure leads to remarkable decreases in the parameters such as TDI, SPI, and repopulation index.…”

In vitrostudy of cypermethrin on human spermatozoa and the possible protective role of vitamins C and E

“…Synthetic pyrethroid insecticides usage has increased lately due to the need to replace common organophosphate insecticides following use restrictions. A consequence of its increased availability, use and broad‐spectrum applicability, there is widespread exposure among the general population (Nesseim et al ., ; Li et al ., ). Diet and household dust are the primary sources of exposure to pyrethroids among nonoccupationally exposed individuals (Julien et al ., ).…”