What is endometriosis?

Endometriosis is a medical condition in which tissue similar to the lining of the uterus (endometrium) grows outside the uterus, typically in the pelvic cavity. This displaced endometrial tissue can adhere to various pelvic organs, such as the ovaries, fallopian tubes, outer surface of the uterus, bowel, or bladder. Endometriosis is a chronic and often painful condition that affects reproductive-age women, typically between their late teens and early 40s, although it can occur in women of any age.


During a woman’s menstrual cycle, the endometrial tissue inside the uterus thickens in preparation for potential pregnancy. If pregnancy does not occur, the uterus sheds this tissue during menstruation. In endometriosis, the tissue that has grown outside the uterus also responds to hormonal changes during the menstrual cycle, thickening and then breaking down and bleeding. However, because this tissue is located outside the uterus, the blood and tissue cannot be shed through menstruation as it would from the uterine lining. Instead, it becomes trapped and can cause inflammation, scarring, and the formation of adhesions (bands of scar tissue) between organs.


The exact cause of endometriosis is not fully understood, but several theories exist, including:


  • Retrograde menstruation: This theory suggests that menstrual blood containing endometrial cells flows backward through the fallopian tubes into the pelvic cavity instead of exiting the body through the vagina during menstruation. These displaced endometrial cells can then implant and grow on pelvic organs.


  • Embryonic cell transformation: According to this theory, hormones such as estrogen may transform embryonic cells into endometrial-like cell implants during puberty.


  • Surgical scar implantation: Endometrial cells may attach to surgical incision sites following procedures such as hysterectomy or cesarean section.


  • Immune system dysfunction: Some researchers believe that abnormalities in the immune system may allow endometrial cells to implant and grow in areas outside the uterus.


What is the relationship between endometriosis and oxidative stress?

The relationship between endometriosis and oxidative stress involves complex interactions between inflammatory processes, hormonal imbalances, and the generation of reactive oxygen species (ROS) within the body. Here’s how oxidative stress influences endometriosis:


  • Inflammation: Endometriosis is characterized by chronic inflammation, which plays a central role in the development and progression of the disease. Inflammatory cytokines, chemokines, and immune cells recruited to endometrial lesions contribute to oxidative stress by promoting the production of ROS and reactive nitrogen species (RNS). ROS/RNS generated during inflammation can induce tissue damage, activate inflammatory pathways, and perpetuate a cycle of oxidative stress and inflammation in endometriotic lesions and surrounding tissues.


  • Hormonal Imbalance: Estrogen is a key hormone involved in the pathogenesis of endometriosis, as endometrial lesions outside the uterus respond to hormonal fluctuations during the menstrual cycle. Estrogen stimulates the proliferation and growth of endometrial tissue, contributing to the formation and progression of endometriotic lesions. Estrogen metabolism generates ROS as byproducts, leading to oxidative stress and DNA damage in endometrial cells. Additionally, estrogen-mediated inflammation and oxidative stress can promote angiogenesis, fibrosis, and adhesion formation in endometriotic lesions.


  • Mitochondrial Dysfunction: Mitochondria are the primary source of ROS production within cells, and mitochondrial dysfunction has been implicated in the pathogenesis of endometriosis. Endometriotic lesions exhibit alterations in mitochondrial function, morphology, and oxidative phosphorylation, leading to increased ROS generation and oxidative stress. Mitochondrial ROS can induce DNA damage, apoptosis, and oxidative modifications of proteins and lipids, contributing to the progression and maintenance of endometriosis.


  • Oxidative Damage: Oxidative stress induces damage to cellular components, including DNA, proteins, lipids, and carbohydrates, leading to dysfunction and structural alterations in endometrial cells and surrounding tissues. Oxidative damage to DNA can result in mutations, chromosomal abnormalities, and genomic instability, which may contribute to the malignant transformation of endometriotic lesions into endometriosis-associated ovarian cancer (EAOC). Additionally, oxidative stress-induced lipid peroxidation and protein oxidation can impair cellular function, disrupt signaling pathways, and promote inflammation and fibrosis in endometriotic lesions.


  • Antioxidant Defenses: The body’s antioxidant defense mechanisms play a crucial role in neutralizing ROS and maintaining redox balance. However, in endometriosis, oxidative stress overwhelms antioxidant defenses, leading to a state of oxidative imbalance. Endometriotic lesions and surrounding tissues may exhibit reduced antioxidant enzyme activity, impaired antioxidant capacity, and alterations in antioxidant gene expression, which contribute to the persistence of oxidative stress and inflammation in endometriosis.


Overall, oxidative stress plays a significant role in the pathogenesis and progression of endometriosis by promoting inflammation, hormonal imbalances, mitochondrial dysfunction, oxidative damage, and impaired antioxidant defenses.