ABSTRACT
In the present work, the effect of exposure to cigarette smoke on male fertility in rats, as characterized by changes in the relative weight of sex organs, epididymal sperm count, activity of marker enzymes and DNA damage was evaluated. Exposure of rats to cigarette smoke caused a gradual decrease in total body weight gain and relative weight of the epididymis and seminal vesicles by 30 and 40% respectively. Epididymal sperm count was reduced significantly by 25% (P 0.05) after 2 weeks and by 41% (P 0.001) after 4 weeks of exposure. Exposure to cigarette smoke had reduced the activity of sorbitol dehydogenase by 18% (P < or = 0.05) and increased the activity of lactate dehydrogenase by 28% (P < or = 0.05). The changes in both key enzymes were significant, which reflected the inhibitory effect of cigarette smoke on spermatogenesis and sperm maturation. The toxic effect of exposure could be explained partially due to induction of DNA damage and oxidative stress as shown by the significant increase in serum 8-hydroxy-2'-deoxyguanosine from 22.83 to 37.33 ng ml(-1) blood.
Subject(s)
Infertility, Male/etiology , Smoking/adverse effects , Sperm Count , Sperm Maturation , Spermatogenesis , 8-Hydroxy-2'-Deoxyguanosine , Animals , DNA Damage , Deoxyguanosine/analogs & derivatives , Deoxyguanosine/blood , L-Iditol 2-Dehydrogenase/metabolism , L-Lactate Dehydrogenase/metabolism , Male , Oxidative Stress , Rats , Rats, Sprague-DawleyABSTRACT
Treatment of male albino rats with 5% honey for 20 days had no significant effect on total body weight or on the relative weight of other organs like the testis, seminal vesicles, spleen, kidneys, liver, heart, or brain. The only significant change was a 17% increase in the relative weight of the epididymis (P < or = .01). The relative weight of all the other organs was similar to those in control animals treated for the same period with drinking water. Treatment of rats for the same period with the same concentration of 5% sucrose produced no significant changes in absolute or relative weight of tested organs compared to control animals. The same treatment with Palestinian honey increased significantly the epididymal sperm count by 37% (P < or = .05). The activity of testicular marker enzymes for spermatogenesis such as sorbitol dehydrogenase (SDH) was increased by 31% (P < or = .05), and lactate dehydrogenase (LDH) was reduced by 48% (P < or = .05), which indicates that treatment with honey induces spermatogenesis. Similar treatment with sucrose had no significant effect on any of the key enzymes or epididymal sperm count. In conclusion, our results show that ingestion of honey induces spermatogenesis in rats by increasing epididymal sperm count, increasing selectively the relative weight of the epididymis, and increasing SDH activity and reducing LDH activity.
