Exploring the Role of Coenzyme Q10 and Cytochrome C Oxidase in Premature Ovarian Insufficiency (POI) : Implications for Treatment and Understanding the Pathogenesis

Abstract

Premature ovarian insufficiency (POI) is a condition in which the ovaries stop functioning prematurely, before the age of 40 (1). Premature ovarian dysfunction or premature ovarian defect, affects approximately 1-2% of women under 40
years of age (2). POI can have varied clinical presentations. It mostly presents with primary or secondary amenorrhea, infertility, hypogonadotropic hypogonadism, or clinical hypo-estrogenism (3). Although it seems like an isolated organ failure, it may show systemic findings due to a sex steroid synthesis defect (1). POI negatively affects many functions, including the individual's psychological state and quality of life. can be caused by a variety of factors, including genetic mutations, autoimmune diseases, and chemotherapy or radiation treatment (4). POI (premature ovarian failure) has many different causes, including spontaneous genetic defects, autoimmune diseases, infections, and medical treatments. However, in many cases, the cause is unknown, and genetics is likely to play a role (5). Coenzyme Q10 (CoQ10) is a vitamin-like substance found in every cell in the body. It plays a vital role in energy production and protects cells from damage (6). Being a cofactor that regulates the expression of genes, CoQ10 is required for signalling, transport, and metabolism in human cells. Deficiency in CoQ10 levels can cause many mitochondrial and oxidative stress pathologies, especially ageing, recessive autosomal mutations, and carcinogenesis (7). Apart from the
above medical conditions, CoQ10 are also lower in people with certain medical conditions, including premature ovarian failure (POF) (8).