HFD- F1 subfertility arises from the susceptibility of the transcriptional network to oxidative stress, resulting in reduced antioxidant properties, motility, sperm-egg binding, and elevated DNA damage. Schematic representation of the HFD-F1 oxidative stress susceptibility to subfertility. Notably, excessive accumulation of ROS surpasses the physiological threshold, thereby damaging PUFAs within the sperm plasma membrane. This oxidative assault affects crucial components such as mitochondria and DNA. Consequently, the sperm's antioxidant defense mechanisms become compromised, leading to a decline in vitality, motility, and fertility.
Keyphrases
- oxidative stress
- dna damage
- high fat diet
- diabetic rats
- ischemia reperfusion injury
- induced apoptosis
- gene expression
- insulin resistance
- heat shock
- dna repair
- metabolic syndrome
- cell death
- type diabetes
- biofilm formation
- adipose tissue
- cell free
- single molecule
- escherichia coli
- circulating tumor
- skeletal muscle
- cystic fibrosis
- physical activity
- candida albicans