Вы находитесь на странице: 1из 15

Ogan Gurel, MD

Biology 301 Lecture #5 Roosevelt University

Ogan Gurel, MD Biology 301 Lecture #5 Roosevelt University Biology 301 Cellular and Molecular Biology Spring

Biology 301

Cellular and Molecular Biology Spring 2002

Lecture # 5: Enzymes

Ogan Gurel, MD

Biology 301 Lecture #5 Roosevelt University

Overall outline

Principles of Chemical Kinetics Enzyme Kinetics Enzyme Regulation

Ogan Gurel, MD

Biology 301 Lecture #5 Roosevelt University

Principles of Chemical Kinetics

Rate Laws Reaction profile Catalysis

Rate Laws

Ogan Gurel, MD

Biology 301 Lecture #5 Roosevelt University

Rate Laws Ogan Gurel, MD Biology 301 Lecture #5 Roosevelt University The rate law is a
The rate law is a function of 1. the rate constant and 2. the concentrations of
 
The rate law is a function of 1. the rate constant and 2. the concentrations of
   
 
The rate law is a function of 1. the rate constant and 2. the concentrations of
The rate law is a function of 1. the rate constant and 2. the concentrations of
The rate law is a function of 1. the rate constant and 2. the concentrations of
 

The rate law is a function of

The rate law is a function of
The rate law is a function of
  • 1. the rate constant and

  • 2. the concentrations of

2. the concentrations of

the

reactants.

reactants.
reactants.
   
The rate law is a function of 1. the rate constant and 2. the concentrations of
The rate law is a function of 1. the rate constant and 2. the concentrations of
 
 
The rate law is a function of 1. the rate constant and 2. the concentrations of
The rate law is a function of 1. the rate constant and 2. the concentrations of
The rate law is a function of 1. the rate constant and 2. the concentrations of
The rate law is a function of 1. the rate constant and 2. the concentrations of
The rate law is a function of 1. the rate constant and 2. the concentrations of
The rate law is a function of 1. the rate constant and 2. the concentrations of
The rate law is a function of 1. the rate constant and 2. the concentrations of
The rate law is a function of 1. the rate constant and 2. the concentrations of
The rate law is a function of 1. the rate constant and 2. the concentrations of
 
The rate law is a function of 1. the rate constant and 2. the concentrations of

Ogan Gurel, MD

Reaction profile

Biology 301 Lecture #5 Roosevelt University

Ogan Gurel, MD Reaction profile Biology 301 Lecture #5 Roosevelt University
Ogan Gurel, MD Reaction profile Biology 301 Lecture #5 Roosevelt University

Ogan Gurel, MD

Catalysis

Biology 301 Lecture #5 Roosevelt University

Ogan Gurel, MD Catalysis Biology 301 Lecture #5 Roosevelt University
Ogan Gurel, MD Catalysis Biology 301 Lecture #5 Roosevelt University

Ogan Gurel, MD

Biology 301 Lecture #5 Roosevelt University

Enzyme Kinetics

Michaelis-Menten Model Enzyme-subtrate interactions Enzyme reaction cycle External effects on enzyme efficiency

Ogan Gurel, MD

Michaelis-Menten Model

Biology 301 Lecture #5 Roosevelt University

Ogan Gurel, MD Michaelis-Menten Model Biology 301 Lecture #5 Roosevelt University  Enzymes are used for
Ogan Gurel, MD Michaelis-Menten Model Biology 301 Lecture #5 Roosevelt University  Enzymes are used for
 

Enzymes are used for the catalysis and control of cell biochemistry.

The Michaelis-Menten model is a general description of simple enzyme kinetics.

At low [S] the rate is first-order with respect to substrate; at high [S] the rate is zero-order (saturated kinetics).

Ogan Gurel, MD Michaelis-Menten Model Biology 301 Lecture #5 Roosevelt University  Enzymes are used for
Ogan Gurel, MD Michaelis-Menten Model Biology 301 Lecture #5 Roosevelt University  Enzymes are used for

Using some simple algebra and approximations show how Michaelis­Menten kinetics reduces to first­order at low substrate concentrations and zero­order at high substrate concentrations.

Enzyme-subtrate

interactions

Ogan Gurel, MD

Biology 301 Lecture #5 Roosevelt University

Enzyme-subtrate interactions Ogan Gurel, MD Biology 301 Lecture #5 Roosevelt University Hexokinase catalyzes the first step
Enzyme-subtrate interactions Ogan Gurel, MD Biology 301 Lecture #5 Roosevelt University Hexokinase catalyzes the first step
Enzyme-subtrate interactions Ogan Gurel, MD Biology 301 Lecture #5 Roosevelt University Hexokinase catalyzes the first step

Hexokinase catalyzes the first step in glycolysis. It is found in all cells including the liver; its

K m is about 30 M.

Glucokinase catalyzes the same reaction, is found exclusively in the liver

and its K m is 10mM. How are the two enzymes different and why are there two of them?

Ogan Gurel, MD

Enzyme reaction cycle

Biology 301 Lecture #5 Roosevelt University

Ogan Gurel, MD Enzyme reaction cycle Biology 301 Lecture #5 Roosevelt University
Ogan Gurel, MD Enzyme reaction cycle Biology 301 Lecture #5 Roosevelt University
 
Ogan Gurel, MD Enzyme reaction cycle Biology 301 Lecture #5 Roosevelt University

External effects on enzyme efficiency

Ogan Gurel, MD

Biology 301 Lecture #5 Roosevelt University

External effects on enzyme efficiency Ogan Gurel, MD Biology 301 Lecture #5 Roosevelt University
External effects on enzyme efficiency Ogan Gurel, MD Biology 301 Lecture #5 Roosevelt University
 
External effects on enzyme efficiency Ogan Gurel, MD Biology 301 Lecture #5 Roosevelt University

Ogan Gurel, MD

Biology 301 Lecture #5 Roosevelt University

Enzyme Regulation

Feedback (negative) inhibition Types of inhibition Inhibition kinetics

Feedback (negative) inhibition

Ogan Gurel, MD

Biology 301 Lecture #5 Roosevelt University

Feedback (negative) inhibition Ogan Gurel, MD Biology 301 Lecture #5 Roosevelt University  Feedback inhibition is
Feedback (negative) inhibition Ogan Gurel, MD Biology 301 Lecture #5 Roosevelt University  Feedback inhibition is
 

Feedback inhibition is a very common regulatory mechanism in biology.

Negative feedback systems are stable systems.

Feedback (negative) inhibition Ogan Gurel, MD Biology 301 Lecture #5 Roosevelt University  Feedback inhibition is
Feedback (negative) inhibition Ogan Gurel, MD Biology 301 Lecture #5 Roosevelt University  Feedback inhibition is
Feedback (negative) inhibition Ogan Gurel, MD Biology 301 Lecture #5 Roosevelt University  Feedback inhibition is
Feedback (negative) inhibition Ogan Gurel, MD Biology 301 Lecture #5 Roosevelt University  Feedback inhibition is
Feedback (negative) inhibition Ogan Gurel, MD Biology 301 Lecture #5 Roosevelt University  Feedback inhibition is
Feedback (negative) inhibition Ogan Gurel, MD Biology 301 Lecture #5 Roosevelt University  Feedback inhibition is

Negative feedback systems are not just confined to enzyme pathways. Show how some of the pituitary­endocrine feedback loops follow the same paradigm. Another example is the relationship between acid secretion and gastrin secretion by parietal cells and antral cells in the stomach.

Ogan Gurel, MD

Types of inhibition

Biology 301 Lecture #5 Roosevelt University

Ogan Gurel, MD Types of inhibition Biology 301 Lecture #5 Roosevelt University
Ogan Gurel, MD Types of inhibition Biology 301 Lecture #5 Roosevelt University

Ogan Gurel, MD

Inhibition kinetics

Biology 301 Lecture #5 Roosevelt University

Ogan Gurel, MD Inhibition kinetics Biology 301 Lecture #5 Roosevelt University  Inhibitors can alter the
Ogan Gurel, MD Inhibition kinetics Biology 301 Lecture #5 Roosevelt University  Inhibitors can alter the
 
Ogan Gurel, MD Inhibition kinetics Biology 301 Lecture #5 Roosevelt University  Inhibitors can alter the

Inhibitors can alter the K m or V max of an enzyme.

Competitive inhibition changes the K m Noncompetitive inhibition changes the V max . Inhibitors can act either non- covalently or covalently. Positive regulation is also possible.

Ogan Gurel, MD Inhibition kinetics Biology 301 Lecture #5 Roosevelt University  Inhibitors can alter the
  • 1. Show how the Lineweaver­Burke plot converts the hyperbolic Michaelis­Menten graph

into a linear one. Why would one use these linear plots?

  • 2. How does aspirin work? What enzyme does it act on? Is it an example of covalent or non­

covalent modification? Does it work via competitive or non­competitive inhibition? Describe its effects on platelet function; what are the clinical implications of its mode of action?

  • 3. How does the antibiotic penicillin work?

Why is penicillin specific to bacteria?

Is it a competitive or non­competitive inhibitor?