scholarly journals Vapor cannabis exposure generationally affects male reproductive functions in mice

2021 ◽  
Author(s):  
Mingxin Shi ◽  
Esther M. Langholt ◽  
Logan C. Butler ◽  
Madeleine E. Harvey ◽  
Emma C. Wheeler ◽  
...  
Keyword(s):  
Dna Damage ◽  
Germ Cells ◽  
Sperm Count ◽  
Plant Matter ◽  
Abnormal Distribution ◽  
Morphometric Analyses ◽  
Drug Naïve ◽  
Neonatal Testis ◽  
Air Control ◽  
Dnmt1 Expression

This study was performed to examine whether vapor exposure to cannabis plant matter negatively impacts male reproductive functions and testis development in mice. Adult CD-1 male mice (F0) were exposed to air (control) or 200 mg of vaporized cannabis plant matter 3x/day over a 10 day period. Subsequently, F0 males were bred with drug naive CD-1 females to generate F1 males, and F1 offspring were used to generate F2 males. Cannabis vapor exposure decreased sperm count and/or motility in F0 and F1 males and disrupted the progression of germ cell development, as morphometric analyses exhibited an abnormal distribution of the stages of spermatogenesis in F0 males. Although plasma levels of testosterone were not affected by cannabis exposure in any ages or generations of males, dysregulated steroidogenic enzymes, Cyp11a1 and Cyp19a1, were observed in F0 testis. In the neonatal testis from F1 males, while apoptosis was not altered, DNA damage and DNMT1, but not DNMT3A and DNMT3B, were increased in germ cells following cannabis exposure. In contrast, the alterations of DNA damage and DNMT1 expression were not observed in F2 neonatal males. These results suggest that cannabis vapor exposure generationally affects male reproductive functions, probably due to disruption of spermatogenesis in the developing testis.

Melatonin attenuates radiofrequency radiation (900 MHz)-induced oxidative stress, DNA damage and cell cycle arrest in germ cells of male Swiss albino mice

2018 ◽  
Vol 34 (5) ◽  
pp. 315-327 ◽  
Author(s):  
Neelam Pandey ◽  
Sarbani Giri
Keyword(s):  
Dna Damage ◽  
Germ Cell ◽  
Germ Cells ◽  
Morphological Changes ◽  
Sperm Count ◽  
Lipid Peroxides ◽  
Sperm Head ◽  
Oxidative Potential ◽  
Swiss Albino Mice ◽  
Albino Mice

Increasing male infertility of unknown aetiology can be associated with environmental factors. Extensive use of mobile phones has exposed the general population to unprecedented levels of radiofrequency radiations (RFRs) that may adversely affect male reproductive health. Therefore, the present study investigated the effect of RFR Global System for Mobile communication (GSM) type, 900 MHz and melatonin supplementation on germ cell development during spermatogenesis. Swiss albino mice were divided into four groups. One group received RFR exposure for 3 h twice/day for 35 days and the other group received the same exposure but with melatonin ( N-acetyl-5-methoxytryptamine) (MEL; 5 mg/kg bw/day). Two other groups received only MEL or remain unexposed. Sperm head abnormality, total sperm count, biochemical assay for lipid peroxides, reduced glutathione, superoxide dismutase activity and testis histology were evaluated. Additionally, flow cytometric evaluation of germ cell subtypes and comet assay were performed in testis. Extensive DNA damage in germ cells of RFR-exposed animals along with arrest in pre-meiotic stages of spermatogenesis eventually leading to low sperm count and sperm head abnormalities were observed. Furthermore, biochemical assays revealed excess free radical generation resulting in histological and morphological changes in testis and germ cells morphology, respectively. However, these effects were either diminished or absent in RFR-exposed animals supplemented with melatonin. Hence, it can be concluded that melatonin inhibits pre-meiotic spermatogenesis arrest in male germ cells through its anti-oxidative potential and ability to improve DNA reparative pathways, leading to normal sperm count and sperm morphology in RFR-exposed animals.

Radiofrequency radiation (900 MHz)-induced DNA damage and cell cycle arrest in testicular germ cells in swiss albino mice

2016 ◽  
Vol 33 (4) ◽  
pp. 373-384 ◽  
Author(s):  
Neelam Pandey ◽  
Sarbani Giri ◽  
Samrat Das ◽  
Puja Upadhaya
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Germ Cell ◽  
Germ Cells ◽  
Sperm Count ◽  
Exposure Period ◽  
Swiss Albino Mice ◽  
Radiofrequency Radiation ◽  
Post Exposure ◽  
Albino Mice

Even though there are contradictory reports regarding the cellular and molecular changes induced by mobile phone emitted radiofrequency radiation (RFR), the possibility of any biological effect cannot be ruled out. In view of a widespread and extensive use of mobile phones, this study evaluates alterations in male germ cell transformation kinetics following RFR exposure and after recovery. Swiss albino mice were exposed to RFR (900 MHz) for 4 h and 8 h duration per day for 35 days. One group of animals was terminated after the exposure period, while others were kept for an additional 35 days post-exposure. RFR exposure caused depolarization of mitochondrial membranes resulting in destabilized cellular redox homeostasis. Statistically significant increases in the damage index in germ cells and sperm head defects were noted in RFR-exposed animals. Flow cytometric estimation of germ cell subtypes in mice testis revealed 2.5-fold increases in spermatogonial populations with significant decreases in spermatids. Almost fourfold reduction in spermatogonia to spermatid turnover (1C:2C) and three times reduction in primary spermatocyte to spermatid turnover (1C:4C) was found indicating arrest in the premeiotic stage of spermatogenesis, which resulted in loss of post-meiotic germ cells apparent from testis histology and low sperm count in RFR-exposed animals. Histological alterations such as sloughing of immature germ cells into the seminiferous tubule lumen, epithelium depletion and maturation arrest were also observed. However, all these changes showed recovery to varied degrees following the post-exposure period indicating that the adverse effects of RFR on mice germ cells are detrimental but reversible. To conclude, RFR exposure-induced oxidative stress causes DNA damage in germ cells, which alters cell cycle progression leading to low sperm count in mice.

Combined action of X-rays and nonylphenol on mouse sperm

2011 ◽  
Vol 6 (3) ◽  
pp. 320-329 ◽  
Author(s):  
Małgorzata Dobrzyńska
Keyword(s):  
Dna Damage ◽  
Germ Cells ◽  
Sperm Morphology ◽  
Sperm Count ◽  
X Rays ◽  
Combined Exposure ◽  
X Ray ◽  
Combined Action ◽  
Sperm Count And Morphology ◽  
Higher Doses

AbstractThe aim of this study was to assess the effects of 2-weeks’ X-ray and/or nonylphenol (NP) exposure on male mice’s sperm count and quality. Pzh:SFIS mice were exposed to X-rays (0.05 Gy, 0.10 Gy, 0.20 Gy) or to nonylphenol (25 mg/kg bw, 50 mg/kg bw, 100 mg/kg bw) or to both agents (0.05 Gy + 25 mg/kg bw NP, 0.10 Gy + 50 mg/kg bw NP). At 24 h and 5 weeks after the end of exposure the sperm count, morphology and frequency of DNA damage in the male germ cells were estimated. Each agent alone diminished sperm count and morphology. The dose of 0.05 Gy of X-rays decreased the frequency of DNA damage. Combined exposure to lower doses of both agents significantly improved sperm morphology and decreased the level of DNA damage compared to one agent alone. Combined exposure to higher doses reduced the frequency of DNA damage compared to the effect of the appropriate dose of NP. Results of combined exposure to low doses of both agents suggest that 0.05 Gy of X-rays stimulate the DNA damagecontrol system and in consequence repair of DNA caused by X-rays and NP. It may be correlated with increased antioxidant capacity.

scholarly journals DNase II mediates a parthanatos-like developmental cell death pathway in Drosophila primordial germ cells

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Lama Tarayrah-Ibraheim ◽  
Elital Chass Maurice ◽  
Guy Hadary ◽  
Sharon Ben-Hur ◽  
Alina Kolpakova ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Germ Cells ◽  
Nuclear Translocation ◽  
Primordial Germ Cells ◽  
Nuclear Accumulation ◽  
Dependent Manner ◽  
Dnase Ii ◽  
Cell Death Pathway ◽  
Parp 1

AbstractDuring Drosophila embryonic development, cell death eliminates 30% of the primordial germ cells (PGCs). Inhibiting apoptosis does not prevent PGC death, suggesting a divergence from the conventional apoptotic program. Here, we demonstrate that PGCs normally activate an intrinsic alternative cell death (ACD) pathway mediated by DNase II release from lysosomes, leading to nuclear translocation and subsequent DNA double-strand breaks (DSBs). DSBs activate the DNA damage-sensing enzyme, Poly(ADP-ribose) (PAR) polymerase-1 (PARP-1) and the ATR/Chk1 branch of the DNA damage response. PARP-1 and DNase II engage in a positive feedback amplification loop mediated by the release of PAR polymers from the nucleus and the nuclear accumulation of DNase II in an AIF- and CypA-dependent manner, ultimately resulting in PGC death. Given the anatomical and molecular similarities with an ACD pathway called parthanatos, these findings reveal a parthanatos-like cell death pathway active during Drosophila development.

scholarly journals Environmental Tobacco Smoke Exposure during Intrauterine Period, Promotes Caspase Dependent and Independent DNA Fragmentation in Sertoli-Germ Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Beril Yüksel ◽  
Sevtap Kilic ◽  
Nese Lortlar ◽  
Nicel Tasdemir ◽  
Semra Sertyel ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Count ◽  
Cigarette Smoke ◽  
Sertoli Cell ◽  
Germ Cells ◽  
Cell Apoptosis ◽  
Smoke Exposure ◽  
Intrauterine Life ◽  
Group 2 ◽  
Group 1

Objectives. To investigate the effect of cigarette smoke exposure during intrauterine period on neonatal rat testis. Methods. Twenty-five rats were randomized to be exposed to cigarette smoke with the Walton Smoking Machine or to room air during their pregnancies. The newborn male rats (n=21) were grouped as group 1 (n=15) which were exposed to cigarette smoke during intrauterine life and group 2 (n=6) which were exposed to room air during intrauterine life. The orchiectomy materials were analyzed with TUNEL immunofluorescent staining for detection of DNA damage. To detect apoptosis, immunohistochemical analyses with caspase-3 were performed. Primary outcomes were apoptotic index and immunohistochemical scores (HSCORES); secondary outcomes were Sertoli-cell count and birth-weight of rats. Results. Sertoli cell apoptosis was increased in group 1 (HSCORE =210.6±41.9) when compared to group 2 (HSCORE =100.0±17.8) (P=0.001). Sertoli cell count was decreased in group 1 (P=0.043). The HSCORE for the germ cells was calculated as 214.0±46.2 in group 1 and 93.3±10.3 in group 2 (P=0.001) referring to an increased germ cell apoptosis in group 1. The apoptotic indexes for group 1 were 49.6±9.57 and 29.98±2.34 for group 2 (P=0.001). The immunofluorescent technique demonstrated increased DNA damage in seminiferous epithelium in group 1. Conclusions. Intrauterine exposure to cigarette smoke adversely affects neonatal testicular structuring and diminishes testicular reserve.

scholarly journals Chronic Exposure to Acrylamide Induces DNA Damage in Male Germ Cells of Mice

2012 ◽  
Vol 129 (1) ◽  
pp. 135-145 ◽  
Author(s):  
Belinda J. Nixon ◽  
Simone J. Stanger ◽  
Brett Nixon ◽  
Shaun D. Roman
Keyword(s):  
Dna Damage ◽  
Germ Cells ◽  
Chronic Exposure ◽  
Male Germ Cells

scholarly journals Germ cell connectivity enhances cell death in response to DNA damage in the Drosophila testis

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Kevin L Lu ◽  
Yukiko M Yamashita
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Germ Cell ◽  
Germ Cells ◽  
High Sensitivity ◽  
Next Generation ◽  
Drosophila Testis

Two broadly known characteristics of germ cells in many organisms are their development as a ‘cyst’ of interconnected cells and their high sensitivity to DNA damage. Here we provide evidence that in the Drosophila testis, connectivity serves as a mechanism that confers to spermatogonia a high sensitivity to DNA damage. We show that all spermatogonia within a cyst die synchronously even when only a subset of them exhibit detectable DNA damage. Mutants of the fusome, an organelle that is known to facilitate intracyst communication, compromise synchronous spermatogonial death and reduces overall germ cell death. Our data indicate that a death-promoting signal is shared within the cyst, leading to death of the entire cyst. Taken together, we propose that intercellular connectivity supported by the fusome uniquely increases the sensitivity of the germline to DNA damage, thereby protecting the integrity of gamete genomes that are passed on to the next generation.

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