Objective: The hypothalamic gonadotropin-releasing hormone pulse
generator, the pituitary gonadotropes, the ovaries, and the uterus play
a crucial role in female fertility. A decline in reproductive
performance represents a complex interplay of actions at all levels of
the hypothalamic-pituitary-ovarian axis. Recently, in the field of
female reproductive aging attention is drawn to the carbonyl stress
theory. Advanced glycation end products (AGEs) contribute directly to
protein damage, induce a chain of oxidative stress (OS) reactions, and
increase inflammatory reactions. Here, we highlight some of the
mechanisms underlying glycation damage in the ovary.
Methods: Searches of electronic databases were performed. Articles
relevant to possible role of OS, AGEs, and receptor for AGE (RAGE) in
aging ovary were summarized in this interpretive literature review.
Results: Follicular microenvironment undergoes an increase in OS with
aging. Data support the role of OS in ovulatory dysfunction because AGEs
are well-recognized mediators of increased OS. RAGE and AGE-modified
proteins with activated nuclear factor-kappa B are expressed in human
ovarian tissue. It was suggested that accumulation of AGEs products at
the level of the ovarian follicle might trigger early ovarian aging or
could be responsible for reduced glucose uptake by granulosa cells,
potentially altering follicular growth. Moreover, impaired methylglyoxal
detoxification causing relevant damage to the ovarian proteome might be
one of the mechanisms underlying reproductive aging.
Conclusions: Further investigation of the role for the AGE-RAGE axis in
the ovarian follicular environment is needed, and results could relate
to assisted reproduction technology outcomes and new measures of ovarian
reserve
