For this presentation, your job in this presentation is to research the drug lovastatin and walk the audience through the cholesterol biosynthesis and how lovastatin inhibits high cholesterol. If lovastatin goes through any structural changes before becoming active, please discuss this. Feel free to use images from the book or the internet to illustrate your point. Presentations should be around 5-10 minutes.

Work of lovastatin in cholesterol reduction:

Explanation:

Cholesterol is necessary for the functioning of all human organs, however it has been associated that there is a relationship between increased blood cholesterol, atherosclerosis and coronary heart disease, thus drugs were developed that decrease cholesterol levels by decreasing also the incidence of myocardial infarction.

Since the 1950s when John Gofman, from the University of California at Berkeley studied the association between coronary heart disease and cholesterol, he discovered that there are more harmful forms of cholesterol called LDL or low-density lipoproteins and another with a protective effect, HDL or lipoproteins of high density, later the Framingham study confirmed this hypothesis, in the following decade in 1960, studies were continued by biochemists Konrad E. Bloch, Feodor Lynen, John Cornforth and George Popják who made them worthy of the Nobel prize by describing the Cholesterol synthesis in four stages, and gained importance in showing that the reduction of HMG-CoA to mevalonate is the main point in maintaining the cholesterol pathway, studies that were completed by Nobel Prize winners Bloch and Lynen.

The high cholesterol content in the diet prevents the simultaneous production of it by the liver, a mechanism regulated by HMG-CoA reductase that catalyzes the conversion of HMG-CoA into mevalonate, an enzyme that, when reduced, can contribute to reducing cholesterol levels. in plasma. Later, after several attempts, the Merck laboratory was able to demonstrate the efficacy of a molecule under the name of lovastatin that produced a significant decrease in plasma LDL levels.

Lovastatin is a selective and competitive inhibitor of the enzyme hydroxymethylglutaryl coenzyme A or HMG-CoA reductase, which catalyzes the reduction of HMG-CoA to mevalonate which is the basis for the formation of sterols and among them the synthesis of cholesterol. Lovastatin in its inactive form is a closed ring of gamma-lactone that, when activated, hydrolyzes to an open ring of β-hydroxy acid, producing a reversible inhibitory binding of HMG-CoA, its main effect is to prevent the formation of mevalonate, an essential component for the formation of cholesterol. In the liver, triglycerides and cholesterol bind to VLDLs and go to plasma to reach peripheral tissues. Low-density lipoproteins (LDL) are created from VLDLs.

Approximately 10% of cholesterol is synthesized in the liver and 15% in the intestine, being carried out in the microsomes and cytoplasm, acetyl-CoA, is a product of oxidation in the mitochondria and by the synthesis of fatty acids is transported to the citoplasma mainly, the process has five important steps:

1. Acetyl-CoAs are converted to 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA)

2. HMG-CoA is converted to mevalonate

3. Mevalonate is converted to the isoprene based molecule, isopentenyl pyrophosphate (IPP), with the concomitant loss of CO2

4. IPP are converted to squalene

5. Squalene is converted to cholesterol.

Lovastatin reduces plasma cholesterol and lipoprotein levels by inhibiting HMG-CoA reductase and cholesterol synthesis in the liver and increasing the number of liver LDL receptors on the cell surface, which in turn increases absorption and catabolism of LDL. Lovastatin reduces LDL production and the number of LDL particles, increases the activity of LDL receptors, decreasing their plasma levels.

Thus today, new molecules continue to be produced with different specific applications, seeking a longer half-life or reduction of side effects, what is certain is that the discovery of lovastatin marks a historical fact for the treatment of cardiovascular disease.

it will take around no amount of ruffe to knock over this 110lbs man because he semms to be around 300lbs. lol

answer:

hi man

explanation: