Homocysteine, a non-proteinogenic sulfur-containing amino acid, was discovered in 1932, and 30 years passed until, in 1969, for the first time, its involvement in pathology was reported. It was only in the last two decades that homocysteine has become a subject of scientific interest and has begun to be intensively studied. A large number of scientists consider homocysteine as an independent risk factor particularly for cardiovascular disease, while others indicate homocysteine as a marker of this disease. Both sides bring scientific arguments for their opinions, yet the dilemma of homocysteine characterization still persists. Although the reported studies do not lead to a unique answer, it is generally accepted that homocysteine is associated with vascular dysfunction. Numerous scientific data show that the link between homocysteine and inflammation is achieved via the reactive oxygen species (ROS) pathway. The latest data indicate hydrogen peroxide as a possible messenger in cellular signaling in physiological or pathological processes and present the consequences of disturbing the oxidation-reducing balance. In this chapter, we present the latest scientific evidences gathered from the literature for both hypotheses regarding homocysteine involvement in pathology, and we propose a possible mechanism of action for homocysteine, based on our preliminary (yet unpublished) work.
Part of the book: Non-Proteinogenic Amino Acids
Both cysteine and homocysteine are sulfur-containing amino acids that play distinct roles in the body. Cysteine is an amino acid that contributes to the synthesis of collagen, a crucial protein for bone structure. Collagen provides the structural framework for bones, contributing to their strength and flexibility. Adequate collagen formation is vital for maintaining bone integrity, and cysteine’s role in collagen synthesis suggests a potential indirect impact on bone health. Elevated levels of homocysteine have been associated with an increased risk of osteoporosis and bone fractures. The exact mechanisms through which homocysteine affects bone metabolism are not fully understood, but it is suggested to involve interference with collagen cross-linking, increased oxidative stress, and altered bone remodeling. The relationship between cysteine, homocysteine, and osteoporosis is intertwined within complex biochemical pathways, constituting a continually evolving area of research.
Part of the book: Cysteine