Can leukocytospermia predict prostate cancer via its effects on mitochondrial DNA?
Rihab DerbelHanen SellamiAhmed RebaiRadhouane GdouraElreavy McelreaveyLeila Ammar-KeskesPublished in: Andrologia (2021)
Leukocytospermia was previously reported to affect sperm quality by the production of reactive oxygen species (ROS) leading to oxidative stress (OS). In turn, OS decreases sperm functional integrity, increases sperm DNA damage and ultimately alters fertility status. To elucidate the impact of leukocytospermia on sperm nuclear DNA integrity and mitochondrial DNA (mtDNA) structure, we conducted a study including 67 samples from infertile patients with low level of leucocytes (Group 1: n = 20) and with leukocytospermia (Group 2: n = 47). In addition to standard sperm parameters' assessment, we measured the levels of inflammation biomarkers [interleukin-6 (IL-6) and interleukin-8 (IL-8)] and evaluated the oxidative status [malondialdehyde (MDA) and enzymatic and non-enzymatic antioxidants]. In addition, we evaluated the level of sperm nuclear DNA fragmentation and analysed mitochondrial DNA (mtDNA) of sperm cells by sequencing of 5 genes [cytochrome oxidase I (COXI), cytochrome oxidase II (COXII), cytochrome oxidase III (COXIII), adenosine triphosphate synthase 6 (ATPase 6) and adenosine triphosphate synthase 8 (ATPase 8)]. As expected, patients with leukocytospermia had significantly higher MDA levels (32.56 ± 24.30 nmole/ml) than patients without leukocytospermia (17.59 ± 9.60 nmole/ml) (p < .018). Also, sperm DNA fragmentation index (DFI) was significantly higher in Group 2 (33.05 ± 18.14%) as compared to Group 1 (14.19 ± 9.50%) (p < .001). The sequencing of mtDNA revealed a high number of substitutions in Group 2 (n = 102) compared to Group 1 (n = 5). These substitutions were observed mainly in COXI. Among COXI substitutions found in Group 2, twelve changes were previously described in patients with prostate cancer and six of them were shown associated with this pathology. These findings suggest that leukocytospermia may predispose to the manifestation of prostate cancer through modification of mitochondrial DNA and this may be promoted by OS.
Keyphrases
- mitochondrial dna
- copy number
- prostate cancer
- oxidative stress
- dna damage
- reactive oxygen species
- radical prostatectomy
- genome wide
- single cell
- induced apoptosis
- circulating tumor
- end stage renal disease
- cell free
- dna methylation
- single molecule
- hydrogen peroxide
- gene expression
- peritoneal dialysis
- cell cycle arrest
- newly diagnosed
- cell death
- cell proliferation
- adipose tissue
- transcription factor
- ejection fraction
- quality improvement
- young adults
- pi k akt
- protein kinase
- diabetic rats
- prognostic factors
- heat shock protein
- bioinformatics analysis