Table 1 The role of oxidative stress in the female reproductive process

Positive effect

Zn-Cu SOD↑ → Promotion of the development of follicles

[26]

Biosynthesis of ovarian steroids → P450↑ → ROS↑ → Blood flow↑ → Rupture of follicles → Ovulation

[36, 37, 40, 41]

ROS↑ → Promotion apoptosis of non-dominant follicles

FSH↑ → E2↑ → CAT and GSH↑ → Protection of cells from apoptosis

[38]

E2 and P ↓ → SOD↓ → OS↑ → Endometrial shedding and implant failure

[62]

ROS↑ → NF-κB↑ → PGF_2α↑ → Luteum dissolution

[35, 39, 61]

Sperm-ovum binding → ROS↑ → Corpus luteus functional↑

ROS↑ → Antioxidants↑ → Synthesis of progesterone

[39]

Negative effect

PCOS:

Serum proline activity↑, OS↑

Physiological hyperglycemia → ROS↑ (Monocytes) → TNF-α↑ → NF-κB↑ → Resistance of Insulin↑

[45, 46]

Preeclampsia:

Defective placenta → Hypoxia and reperfusion injury → OS↑ → Cytokines↑, Prostaglandins↑ → TAS↓, GPx of placenta↓

V_C↓ → Risk of preeclampsia↑

(MDA↑) ROS↑ → Vasoconstriction↑ → Coagulation activity↓

OS↑ → Vascular endothelial injury↑ → ROS↑ → TNF-α↑, ox-LDL↑ → Endothelial subtypes of activated NAD(P)H oxidase → SO anion↑

Auto-antibodies of AT1-AA↑ → NAD(P)H oxidase↑ → ROS↑ → SO anion↑

[67, 76,77,78,79,80,81, 83,84,85]

Endometriosis:

In the peritoneal fluid, MDA↑, IL-6↑,TNF-α↑, IL-8↑, VEGF↑, MCP-1↑, ox-LDL↑.

In endometriotic lesions: OS↑ → NF-κB↑ → Inflammation↑

In endometriotic cells: MAPK↑

ROS↑ → IUGR, abortion, fetal malformation

[71,72,73, 75]