As opposed to subjects homozygous for the wild-type AA allele the CC homozygotes demonstrated a diminished LDL D decline upon treatment with atorvastatin. Consequently, to recognize the most p53 ubiquitination responsive people for the CYP7A1 specific drugs, a knowledge of the CYP7A1 genotype and basal amount of the enzyme activity will likely be required. The latter will soon be especially essential for subjects who do not have polymorphisms in CYP7A1 to serve as an indicator of lifestyle and nutritional preferences. Direct measurement of cholesterol 7 hydroxylation is difficult because CYP7A1 is barely expressed in the liver, while genotyping becomes a routine procedure in medical practice. Liver biopsies are necessary to undertake the enzyme assay. Plasma levels of the merchandise, 7 hydroxycholesterol, were proven to reflect the activity of CYP7A1. However, 7 hydroxycholesterol might be established non enzymatically and is measured by high priced and sophisticated techniques according to isotope dilution mass spectrometry. Another sterol, 7 hydroxy 4 cholesten 3 one, formed enzymatically from 7 hydroxycholesterol was tested and proved to be the right marker for CYP7A1 activity and bile acid synthesis, to overcome these limitations. Ergo, to better understand the potential of CYP7A1 being a target for cholesterol-lowering, further studies are required by which known modulators of Mitochondrion CYP7A1 activity, both positive and negative, are evaluated for their effect on serum lipids based on the knowledge of CYP7A1 genotype and enzyme activity. 4. 2. CYP27A1 Under normal circumstances, the process of bile acid biosynthesis started by CYP27A1 accounts for elimination of only 18 20 mg cholesterol/day. That pathways, usually Bortezomib PS-341 named as alternative, begins in extrahepatic tissues and matches the HDL mediated reverse cholesterol transport. . When the classical pathway is suppressed this alternate pathway becomes upregulated. Studies of someone with total CYP7A1 deficiency demonstrated that he had a 2 fold enhanced CYP27A1 activity compared with control subjects carrying no mutation in CYP7A1. CYP27A1 converts cholesterol to 27 hydroxycholesterol. This oxygenation reaction is suggested to be very important to cholesterol elimination from human lung macrophages and cells in arterial endothelium. CYP27A1 can also be involved in the classical pathway of bile acid biosynthesis in the liver, where it hydroxylates bile acid intermediates. The products of CYP27A1 actions 27 hydroxycholesterol and 3B hydroxy 5 cholestenoic acid will be the ligands for the nuclear liver X receptors. Yet, a few lines of proof argue against a regulatory role of CYP27A1. Deficiency of the enzyme activity due to mutations in CYP27A1 contributes to a slowly progressive disease cerebrotendinous xanthomatosis, which can be characterized by a number of manifestations. One of them is premature atherosclerosis. Individuals with CTX normally have normal plasma levels of cholesterol, however, cholesterol and cholestanol are gathered in nearly every tissue.