Phase II Detoxification – Enzymatic Conjugation : Following phase I transformation, the original lipid-soluble toxin has been converted into a more water-soluble form, however, this reactive intermediate is still unsuitable for immediate elimination from the cell for a couple of reasons: 1) phase I reactions are not sufficient to make the toxin water-soluble enough to complete the entire excretion pathway; and 2) in many cases, products from the phase I reactions have been rendered more reactive then the original toxins, which makes them potentially more destructive than they once were. Both of these shortcomings are addressed by the activities of the phase II enzymes, which modify phase I products to both increase their solubility and reduce their toxicity. The activation of the phase II enzymes is responsible for the anti-mutagenic and anti-carcinogenic properties of the metabolic detoxification systems; it is widely accepted that phase II enzymes protect against chemical carcinogenesis, especially during the initiation phase of cancers. 24
Q. My muscle enzymes are at 355, my DR says normal is 200. She refered me to a Neurologist. What could be wrong? I am experiencing sore legs when I walk, weakness, and sometimes difficulty in swallowing. I am 46 I had a minor heart attack 5 yrs ago with a stent placed in my LAD. I am on Crestor 10mg. my Dr. has adjusted the dosage several times and used other drugs but it doesn't change the results much if at all. A. Crestor itself may cause elevated muscle enzymes (you probably refer to Creatine Kinase, http:///wiki/Creatine_kinase). However, weakness and swallowing problems may raise the suspicion of a disease of the nerves or muscles.
As indicated in the Figure above showing the pathway of cholesterol biosynthesis a molecule of geranylpyrophosphate (GPP) and a molecule of isopentenylpyrophosphate (IPP) are condensed into farnesylpyrophosphate (FPP) through the action of the farnesyl diphosphate synthase enzyme which is encoded by the FDPS gene. Through the action of the ER-localized enzyme, dehydrodolichyl diphosphate synthase (encoded by the DHDDS gene), farnesylpyrophosphate is elongated via the sequential head-to-tail addition of multiple isopentenylpyrophosphate groups in a reaction referred to as cis -prenylation. The number of IPP substrates added ultimately determines the overall number of isoprene units in dolichol which in humans ranges from 17 to 21. The DHDDS gene is located on chromosome and is composed of 10 exons that generate five alternatively spliced mRNAs each of which encode a distince protein isoform. The product(s) of the DHDDS reaction is referred to as a polyprenolpyrophosphate. The pyrophosphate is removed by an as yet uncharacterized enzyme activity that may be either a polyprenol pyrophosphate phosphatase or a polyprenol phosphatase resulting in the formation of a polyprenol.