# Impact of Tobacco Smoke Exposure on Male Fertility: An In Vivo Study Using Drosophila melanogaster

## TL;DR

Tobacco smoke exposure in male fruit flies reduces offspring fertility and lifespan, with greater effects in flies lacking DNA repair abilities.

## Contribution

This study demonstrates genotype-dependent reproductive toxicity of tobacco smoke using Drosophila as an in vivo model.

## Key findings

- Paternal tobacco smoke exposure impairs fertility, prolificacy, and offspring longevity in both wild-type and DNA repair-deficient Drosophila strains.
- DNA repair-deficient mus308 males show higher sperm cytotoxicity and greater reduction in sperm count after smoke exposure.
- Exposure leads to increased morphological abnormalities in spermatozoa of DNA repair-deficient males.

## Abstract

What are the main findings?
Paternal tobacco smoke exposure significantly impairs the fertility, prolificacy, and longevity of offspring of two strains of Drosophila melanogaster: Oregon K (a wild-type strain proficient in all major DNA repair pathways) and mus308 (a DNA repair-deficient strain).The DNA repair-deficient mus308 strain showed higher vulnerability to spermatozoa cytotoxicity and a greater magnitude of reduction in spermatozoa count.

Paternal tobacco smoke exposure significantly impairs the fertility, prolificacy, and longevity of offspring of two strains of Drosophila melanogaster: Oregon K (a wild-type strain proficient in all major DNA repair pathways) and mus308 (a DNA repair-deficient strain).

The DNA repair-deficient mus308 strain showed higher vulnerability to spermatozoa cytotoxicity and a greater magnitude of reduction in spermatozoa count.

What is the implication of the main finding?
The reproductive toxicity of tobacco smoke is genotype-dependent, suggesting that compromised DNA repair pathways exacerbate the transgenerational impact of environmental toxicants.D. melanogaster is a robust and sensitive in vivo model to mechanistically evaluate the paternal reproductive risks and transgenerational effects of complex smoke-related compounds.

The reproductive toxicity of tobacco smoke is genotype-dependent, suggesting that compromised DNA repair pathways exacerbate the transgenerational impact of environmental toxicants.

D. melanogaster is a robust and sensitive in vivo model to mechanistically evaluate the paternal reproductive risks and transgenerational effects of complex smoke-related compounds.

Tobacco smoke has been consistently associated with impaired spermatozoa quality in men, including decreased concentration, motility, and increased morphological abnormalities. Key tobacco-related toxins such as nicotine and cadmium induce oxidative stress, leading to DNA damage in germ cells. This study aimed to evaluate the effects of tobacco smoke exposure on male fertility using Drosophila melanogaster as an in vivo model. Fertility, fecundity, parental toxicity, lifespan, and spermatozoa morphology were assessed in two strains: the wild-type Oregon K and the DNA repair-deficient mus308. Males were exposed to whole-tobacco smoke in a controlled environment for periods of 0, 1 and 7 min. Tobacco smoke exposure reduced fertility, fecundity, and offspring longevity in both strains. Additionally, spermatozoa from mus308 males exhibited a higher frequency of morphological abnormalities. These findings demonstrate the detrimental impact of tobacco smoke on male reproductive function and suggest increased vulnerability in organisms with impaired DNA repair capacity.