Bio & Chem In The Modern World

Front 1

What are the 4 characteristics of genetic Material?

Back 1

1) storage of information 2)expression of information 3)variation by mutation 4)ability for replication of information

Front 2

What did Fredrich Meischer accomplish?

Back 2

He separated nuclei from cytoplasm and isolated an acidic substance called nuclein. Nuclein contained large amounts of phosphorous but little sulphur.

Front 3

Why did people think proteins were genetic material and not nucleic acids?

Back 3

Proteins are very abundant and varied. They contain 20 amino acids whereas nucleic acids are composed of only 4 nucleotides (A, C, T and G)

Front 4

What did Rosalind Franklin discover/accomplish?

Back 4

She studied DNA crystals using X-rays and recognized A and B forms of DNA

Front 5

In which phase is DNA replicated?

Back 5

S phase

Front 6

What did Arthur Kornberg do?

Back 6

-He purified DNA replication factors from E Coli
-He reconstituted DNA synthesis reaction in vitro
He won Nobel Prize with S. Ochoi in 1959 for work on the biochemistry of DNA synthesis

Front 7

What are 3 causes of cancer?

Back 7

1) Bad luck (Mistake is made during DNA replication and not repaired) 2)Bad genes 3)Environmental factors like a)carcinogens b)viruses

Front 8

What are carcinogens?

Back 8

Chemicals that promote cancer

Front 9

What are 3 things that carcinogens do?

Back 9

1) React with DNA [ex: nitrogen mustards adn UV light] 2)Form a new molecule in the body that reacts with DNA [ex: Benzopyrene] 3) Increase risk of cancer w/o affecting DNA [ex: phorbol esters]

Front 10

What are 3 common types of DNA damage?

Back 10

1) Depunination 2)Deamination 3)Thymine Dimer Formation

Front 11

What does UV light do that causes skin cancer?

Back 11

It causes adjacent T's and C's to become connected with covalent bonds

Front 12

What is Xeroderma pigmentosum?

Back 12

-Rare, recessive mutations
-High incidence of skin cancer
-Very sensitive to sunlight
-Defects in proteins prevents repair of UV damage
-Limited treatment

Front 13

How do phorbol esters increase the risk of cancer?

Back 13

They activate a signaling protein called PKC. PKC regulates many cellular processes. The activation of PKC leads to uncontrolled cell growth, which leads to cancer.

Front 14

What are 3 ways cancer can be treated?

Back 14

1) Surgery 2) Radiation 3)Chemotherapy

Front 15

What are 3 challenges to chemotherapy?

Back 15

1) Cancer cells mutate quickly 2)Chemotherapies often require correct functioning of cell system control proteins, which may be mutated in cancer cells 3)Only one surviving cell can cause cancer to recur

Front 16

What is the difference between non selective and selective chemotherapy?

Back 16

Selective has fewer side effects. However, both types are not always effective, and there can be resistance.

Front 17

What are 2 examples of non selective chemotherapy?

Back 17

Nitrogen mustards and 5-fluorouracil

Front 18

What are 2 examples of selective chemotherapy?

Back 18

Tamoxifen and Gleevec

Front 19

What is the goal of non-selective chemotherapy? What are side effects?

Back 19

The goal is to prevent cell divison. Side effects: Kill healthy dividing cells (Hair, stomach lining, immune cells)

Front 20

What are 2 ways to prevent cell division?

Back 20

1) Damage DNA-prevent DNA replication 2) Prevent synthesis of key components of cell division-ie, DNA nucleotides

Front 21

How does Nitrogen Mustard Stop Cell Divison?

Back 21

Cell senses modified DNA and cannot repair. Triggers cell suicide (apoptosis). If this sensing mechanism fails-it can lead to cancer.

Front 22

What is the mechanism of 5-Fluorouracil?

Back 22

It inhibits an enzyme called thymidylate synthase.
5 Fluorouridine monophosphate binds to thymidilate synthase 1000 fold better than uridine monophosphate. A covalent bond is formed with 5-FU which can't be broken-enzyme is destroyed. No more Ts are made for DNA synthesis-signals cell suicide.

Front 23

What does thymidylate synthase do?

Back 23

It makes Ts for DNA synthesis.

Front 24

What is the goal of selective inhibitors in breast cancer?

Back 24

To treat tumors by inhibiting the action of estrogen. To prevent the synthesis of estrogen.

Front 25

How do SERMS interact with estrogen receptors?

Back 25

-Binding of SERM results in a different structure.
-This structure may or may not be recognized by coactivator proteins.

Front 26

What is the mechanism of Gleevec action?

Back 26

It inhibits a tyrosine kinase oncogene?

Front 27

What is the function of some tyrosine kinases?

Back 27

-growth factors signals receptor in cell membrane to dimerize
-receptor dimer is activated, becoming phosphorylated
-activation signal gets transferred down a cascade of enzymes
-in nucleus genes get turned on (become transcribed) that cause cell to divide

Front 28

Why is there resistance to chemotherapies?

Back 28

1) Cancer cells are prone to mutations 2) If one cell is resistance and survives, the cancer will return 3) The cellular processes that enable chemotherapies to work are the ones most likely to be mutated in cancer 4) The cell can develop proteins that can pump out all small molecule drugs

Front 29

What are some ways the plague can be transmitted?

Back 29

-Bite from rodent flea carrying plague bacterium
-Handling infected animal (black house rat)
-Plague enters human body through lesions of skin or through mucous membranes of nose of throat

Front 30

What is The Lethal Factor?

Back 30

A protease that destroys cellular kinsaes. This activity can lead to cell death.

Front 31

What does The Edema Factor do?

Back 31

It causes levels of cAMP to rise in the cell. This leads to fluid outpour into extracellular spaces, resulting in edema, or swelling.

Front 32

What are the 4 basic concepts Ehrlich introduced?

Back 32

1) Screen many compounds for killing bacteria 2) Quantitate therapeutic vs. toxic dose 3) Similar compounds act similarly 4) A prodrug is a drug metabolized to active form in body

Front 33

What were 3 treatments for victims of the Coconut Grove Fire?

Back 33

1) Blood plasmid-prevent dehydration 2) Sulfa drugs-prevent blood poisoning 3) Penicillin

Front 34

What is the mechanism of Penicillin?

Back 34

It prevents cell wall biosynthesis.

Front 35

How does penicillin inhibit transpeptidase?

Back 35

A covalent bond is formed between penicillin and transpeptidase. Thus, transpeptidase is no longer able to catalyze other reactions.

Front 36

What did William Roberts observe?

Back 36

Cultures of the mold Penicillin glaucum did not exhibit bacterial contamination.

Front 37

What did Pasteur and Joubert observe?

Back 37

Growth of the anthrax bacilli was inhibited when the cultures became contaminated with mold.

Front 38

What did Lister observe?

Back 38

Samples of urine contaminated with mold did not allow the growth of bacteria.

Front 39

What does erythromycin do?

Back 39

It binds to RNA and blocks the exit of protein from ribosome.

Front 40

What are some uses of antibiotics in the modern world?

Back 40

-Treatment of many diseases of domestiated animals
-Preservation of food
-Preservation of certain wines, beers, and cheeses
-Preservation and purification of virus preparations and other biologial materials
-Treatment of certain plant diseases

Front 41

What are some examples of the misuse of antibiotics?

Back 41

-Often the wrong antibiotic is prescribed
-Unneccessary distribution

Front 42

What are the 3 biochemical basis of resistance?

Back 42

1) Production of enzymes that destroy or inactivate the antibiotic
2) Prevention of access for the antibiotics (efflux pumps)
3) Modification of target site or enzyme

Front 43

What are 3 methods of genetic transfer?

Back 43

Transformation, Conjugation, and Transduction