Exam III final cut Flashcards
Oxygen is reactive/combustable in very
high temp
How are ROS formed?
• Oxygen reacting with a decompartmentalized metal ions, known as the Fenton or Haber-Weiss reaction
How do ROS damage cells?
Cell membrane contains a lot of polyunsaturated fats which are highly reduced = prone to oxidation by ROS.
OH radicals attack DNA and damage pyrimidines, purines, and deoxyribose backbone which is highly susceptible to oxidation
Physiological functions of ROS
Cells of the thyroid make H2O2 to attach iodine atoms to thyroglobulin = thyroxine
Macrophages and neutrophils must generate ROS in their granules to kill some types of bacteria during phagocytosis.
Defense mechanisms against ROS
There are 1. Preventative mechanisms 2. Repair mechanisms 3. Physical defenses. Antioxidant defense (enzymatic defense) Superoxide dismutase (enzyme) converts two superoxide anions into H2O2 and oxygen. Catalase (enzyme): converts H2O2 to water and O2. Small Molecules are antioxidants: Vitamin A,C,E, Uric Acid Glutathione peroxidase: reduces lipid peroxides through oxidizing glutathione. Glutathione is very important to ROS defense
Markers of liver disease
Mild liver disease: Typically no outward symptoms. Detected only as biochemical changes
Severe liver Disease: Yellow pigmentation, bruising readily, profuse bleeding, abdomen distended with fluid
Can lead to Endocrine, CNS, skin, cardiovascular, and GI problems
Liver plasma proteins
Most plasma proteins synthesized by the liver and include albumin, acute phase proteins, coagulation factors, and alpha and beta plasma globulins
Acute phase protein
C-reactive proteins are seen (are released) due to damaged tissues and infections and are best index of acute phase protein response
Drug metabolism in the liver
Most drugs are metabolized in the liver through the addition of a polar head group to drug. This is done by P-450 cytochrome drug detoxification enzymes.
Acetaminophen toxicity
When acetaminophen is taken in therapeutic doses it is conjugated to glucuronic acid and excreted. In excess, free radical-mediated peroxidation of liver membrane lipids occurs resulting in hepatocellular damage
Alcohol toxicity
Ethanol is oxidized in the liver, mainly by alcohol dehydrogenase, to form acetaldehyde, which is in turn oxidized by aldehyde dehydrogenase (ALDH) to acetate. Acetaldehyde and acetate are toxic to the body.
Phases of insulin production after oral glucose
First phase is from glucose stimulation, then by amino acids through stimulation of the vagus nerve and hormones secreted by the gut
Function of epinephrine in energy metabolism
• Energy is provided from glucose, fatty acid, and protein catabolism. In times of stress, anti-insulin hormones are produced. Anti-insulin hormones include Epinephrine, cortisol and glucagon. These anti-insulin hormones, like epinephrine, can be used to decrease anabolism (glycogen synthesis), and increase catabolism (glycogenolysis, lipolysis, and proteolysis and increased insulin-dependent glu. Uptake) Glycogenolysis is the conversion of glycogen to glucose for energy use.
Ketoacidosis and type 1 diabetes
• Ketone bodies accumulate in plasma. Increasing blood H+ thus lower blood pH = diabetic ketoacidosis
A1C test
• Hemoglobin can be modified by binding to glucose (glycation). The degree of glycation is an indicator of glucose exposure over the RBC lifespan. Normal A1c is 4-6%. Thus testing A1c can indicate diabetes.
- Know about the similarities between developmental genes from different organisms.
Different organisms can have homologous genes that can function interchangeably. I.e. Example of a mouse that lacks Engrailed-1 gene won’t have a cerebellum but if you transplant that from a fruitfly then the mouse can still develop a cerebellum.
homeotic genes direct regions (segments) to
differentiate into their final forms.
genes can have complex expression patterns by having a series of
control regions directing transcription in different regions of the organism.