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Effect of Smoking on DNA Methylation in Spermatozoa

by Scienceooze
Smoking on DNA Methylation

Smoking on DNA Methylation

Multiple health aftermaths of tobacco smoking have been reported and male fertility has also been observed to be affected by tobacco exposure.

Studies have reported that pre-conception paternal smoking could increase the morbidity rate of offspring because smoking interferes with DNA methylation and these epigenetic modifications pass to progeny via spermatozoa.

Tobacco smoke comprises of more than 4000 chemicals including carcinogens, responsible for the increased risk of cardiovascular diseases, different cancers and respiratory tract dysfunctions.

Smoking is responsible for the accumulation of cadmium and lead in seminal plasma which reduces the sperm count and motility. In a study, human and mice have been exposed to tobacco smoke, increased sperm chromatin structural abnormalities and sperm DNA damage, and reduced reproductive potential have been reported in them.

Significant increase in the sperm DNA mutations at expanded simple tandem repeats (ESTR) and anomalies in chromatin structure have also been reported in smoke-exposed mice. It also has been observed that germline cells are more susceptible to genetic or epigenetic disgrace resulting from smoke exposure than somatic cells.

Several studies were conducted to check the different semen parameters and DNA damage in smokers and non-smokers. The decrease in several semen parameters including semen volume, total sperm count, and total progressively motile sperm count in men who smoke compared with never smokers were observed. More, a marginally significant increase in sperm DNA damage in men who smoke was identified.

But the smoking duration or amount did not influence the level of DNA damage. Sperm DNA methylation fidelity can be disrupted to some extent that results in less tightly controlled sperm DNA methylation patterns which also seem to vary among patients.

Pre‐conception paternal smoking has been related with increased chances of various disorders in offspring including different forms of cancer and birth anomalies. Global methylation levels do not seem to be different in men who do and do not smoke also histone‐bound regions may be more susceptible to methylation agitations compared with protamine‐bound regions.

It is important to note that modified sperm DNA methylation at histone‐bound loci may be more poignant on gene expression because of the vitality of such regions in early embryonic development.

In concluding remarks, as we have already known that smoking does alter the DNA methylation patterns but we also know that in early embryonic stages all epigenetic marks are re-established after removing in a tissue-specific manner, so in order to impact the offspring these alterations by smoking should pass to offspring without being removed in epigenetic reprogramming, but if on the other hand, these changed DNA methylations could not pass to offspring then they might have an impact on early embryonic gene expression. These are hot areas of future research.

By: Gulfam Mushtaq, BS (Hons.) Biotechnology, University of Veterinary and Animal Sciences, Lahore

Contact: gulfammushtaq7667@gmail.com

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