The homocysteine hypothesis states that circulating homocysteine is a vascular toxin in concentrations that occur in the general population and in renal failure.
Thus, these evidences indicated that PCS was not only a vascular toxin but also a nephrotoxin.
Since haemolysis acts as a vascular toxin and is likely to be a cause of vascular destruction, it is thought to be the direct cause of irreversible TBF stasis.
Paraoxonase, although studied most extensively because of its ability to detoxify organophosphate insecticides (James 2006; van Himbergen et al. 2006), has drawn increasing attention because it hydrolyzes homocysteine thiolactone, a vascular toxin that inhibits copper enzymes (Klevay 2006).
Although hepatic fibrosis in humans can be caused by various stimuli (congenital, metabolic, inflammatory, parasitic, vascular, toxins or drugs), the molecular mechanisms underlying fibrosis are basically the same [ 3].
This review evaluated the effectiveness of pre-, pro- and synbiotics on reducing a nephro-vascular uremic toxin, indoxyl sulphate (IS), involved in cardiovascular disease in chronic kidney disease.
Intrinsic processes affect hepatic cellular function (e.g. infections, metabolic disorders, endocrinopathies, chromosomal abnormalities, vascular abnormalities, toxins, neoplasms, and prematurity) [ 2].
Under physiological conditions, the NVU regulates nutrient supply, vascular growth, hemodynamics, toxin elimination and brain protection.
Early hypotheses of causal factors of the disease examined vascular trematodes and toxins but results were inconclusive [7], [8].
This may be due to anatomical uterine defects, chromosomal defects, parental chromosomal rearrangements, gene mutations, endocrine factors, sub clinical infections, environmental toxins, collagen vascular diseases, auto immune factors, and psychological trauma or stress.
Elevated homocysteine levels have long been associated with ASCVD (for example, [ 3]) and homocysteine is a direct toxin for the vascular endothelium.
