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some less familiar bio concepts

prokaryote bacteria shape

spherical -Cocci ex: staph
rod-like -bacilli ex: e coli

prokaryote cells have

cell membrane, cytosol, plasma membrane, cell wall (which only euk plants/fungi have), nuclear area (not a nucleus though) and Ribosomes!

cytoskeleton size in order

(actin) microfilaments< intermediate filaments< microtubules

what is different about plants as euks?

cell wall (outside the cell membrane for rigidity)
chlorophyll (4 photosynthesis)

what happens in the nucleolus?

rRNA synthesis

Ribosome role

protein factories
can be free or bound

role of Golgi

signaled by E.R. to repackage products and release in exocytosis outside the cell

ER location? why?

right outside nucleus
shipping center
smooth -no ribs-->lipid synthesis & detox drugs/poisions
rough -ribosomes-->produce protein products

what does Golgi wrap things in?

in plants these are called Vacuoles

hormone entry into cells : nonpolar vs polar

nonpolar steroid hormones =lipid soluble-->diffuse thru mem
later meet up with their receptor which in the cell
polar steroid hormones=protein/peptide -->bind to extracell receptor ->modify cell activity via internal 2nd messenger cAMP


-contains DNA which
1)directs protein synthesis
2)serves as genetic blueprint during cell respiration

what do lysosomes do?

they use hydrolytic enzymes pH 5 to break down matl brought in by Endosomes (garbage trucks)
-they remove old cell competenets/replace w/new ones
-if DNA/nuc is damaged-->autolysis

Mitochondria-diff parts/role

mit matrix=where enzymes 4 cell respiration are
i.m.m=rxy chamber 4 e- TC
outer=selects entry molecules

mitochondria (why diff?)

semiautonomous (probs evolved from prokaryote have own genes and rep. indy of nuc via Binary fission)
->inherited from Mother (if defected-all kids get it )


specialized factories w/digestive enzymes transform and breakdown fats

diff types of microbodies

1) peroxisomes-make H2O2 -breakdwn fats-detox rxns liver
2)glyxoxysomes-in plants, convert fats->usable fuel=sugar
until plant can make NRG via photosynthesis


have chlorophyll generates NRG w H20 CO2 and Sun
"solar power plants"

diff about chloroplasts?

have their own DNA -evolved via symbiosis

Cell Wall -diff in diff organisms

plants- cellulose fungi-chitin
role=outside cell membrane incr defense and stability

what are centrioles?

special type of Microtubules that are involved in spindle formation (cell div) -form spindle on which chroms move
-come in pairs at right angles to e.o
-not in plants
-determine position of nucleus and spatial arrangement in cell


highway system that helps with transport in cell

micro filaments

actin smallest/thinnest
-musc contraction (interact w myosin)
-matl mment in cell membrane and ameboid mment

intermediate filaments

maintain overall integrity of cytoskeleton


largest cytoskel made of hollow tubulin polymers
struct basis 4 cilia and flagella (trap and sperm motility)
involved in chrom sep in mit/meiosis (bc centrioles are a class of microtubules)

passive diffusion entry modes

simple diffusion, osmosis , facilitated diffusion
(all go down conc gradient)

facilitated diffusion

especially helpful for many large polar molecules and ions impeded by the lipid bilayer of a membrane diffuse passively with the help of transport proteins that span the membrane

what areas of body use active transport across cell

nervous system (to maintain electropotl gradient in neurons)
kidneys (conserve useful solutes (glucose) from filtrate


endocytosis of small particles


endocytosis of big particles

cells of nervous tissues



can be s.s,d.s RNA or DNA circ or linear
obligate intracellular parasites (need to enter a cell to infect)

virus makeup

composed of nucleic acids surrounded by a protein coat (capsid)

obligate intracell parasites

describes virus' need to replicate genetic info within a cell bc they lack the necess machinery to do it themselves (unlike bacteria which mustnt enter cell)
-they highjack a cells machinery and replicate new copies-virions


new copies made by virus once it's high-jacked a cell which can be released to infect new cells
-they alter orders of the nuclues to make their own nefarious products


viruses that specifically target bacteria (just inject their genetic material in them leaving the remaining structures outside )


ph 7.4 37* optimal
induced fit> lock key such that sub and enzyme change confirm


use no cofactors


need cofactors (metal ions or coenzymes=organic groups or vitamins)

enzyme kinetics affected by

concentration, temperature and pH

if (enzyme) > (substate)

rxn velocity goes up

as (substrate) increases,

rxn rate speeds up but at a negative rate (concave down)
-eventually no active sites left on enzymes-saturation (vmax)


Vmaz reached such that there are no remaining active sites left on enzymes (so adding substrate wouldn't make a diff)

1/2 max

1/2 enzymes active sites are full continues to speed up but not by Km=(Substrate)

Km value

if (S) > Km, approaching Vmax so adding S wont greatly affect rate
if (S)<Km adding (S) will greatly affect rxn rate

what does value of Km mean

low Km-high affinity of enzyme for substrate (so you need less (S)
high Km- low affinity of enzymes for substrate

rxn rate and temp relation

as temp inc 10*, rate doubles until opt 37 (after which denatur)

pH and rxn rates for enzymes

7.4 is best for human blood (7.3=acidosis)
-dec in stomach (pepsin=2 is max )
-inc in S.Int (pan enzyme=8.5)


multiple binding sites

allosteric activator

makes active sites more avail

allosteric inhibitor

makes active sites less avail

Feedback inhibition

product binds to enzyme that acted earlier in path making the enzyme not available to substrate ex:hormones
(this one is distinctive bc it is the PRODUCT that inhibits)

reversible inhibition

competitive -solve:add more substrate
noncompetitive- (inhibit) binds to site:adding won't solve

irreversible inhibition

active site is made permanently unavailable bc enzyme is permanently altered
(this one is distinctive bc it is @ active site)


inactive enyzmes released w/ a catalytic and regulatory domain which must be altered chemically to expose active site (released inactive bc can damage cell)
ex: trypsinogen,pepsinogen, capsases,angiotensinogen,chymotrypsinogen)


zymogens that cause apoptosis

autotrophs use

suns energy to prod glucose in which they store NRG
anabolic process (make up)
they do endotherm process of photosynthesis)


liberate NRG by breaking bonds in glucose in
catabolism (cut up/break up)
to release NRG in exothermic proc of Cellular respiration


adenine triphosphate -primary energy currency of cell
-rapidly formed and degraded to allow energy to be stored or released as needed
-generate during glucose catabolism(cell respir)
actual NRG is stored in the phosphate groups (many - charges in close proximity)

why does breaking ATP release alot of usable energy?

bc phosphate groups are close and neg charges dont like being next to e/o so this is alot of energy

does ATP have deoxyribose or ribose sugar?

-ATP has ribose group (not deoxyribose) bc the sugar part has OH rather than just a H like on deoxyribose

where does glycolysis occur


where does fermentation occur


where does the TCA cycle occur

Mitochondrial matrix

where does the pyruvate-->acetyl coA occur?

mitochondrial matrix

e- Transport chain occurs

Inner mitochondrial matrix

NADH gives

3 ATP/molecule
except in cytoplasm where it gives 2ATP/molecule


gives 2 ATP per molecule

final e- acceptor


when is fermentation used

after glycolysis in anerobic conditions
reduces pyruvate to ethanol or lactic acid

alcohol fermentation

pyruvate (2 3Cs ) -->Co2+Acetalaldehyde (3C)
-->Acaetaldehyde +NADH+H+-->Ethanol (2C)+NAD+

lactic acid fermentation

pyruvate builds reduced to lactic acid (3C)
pyruv (3C)+NADH+H+->Lactic Acid+NAD+
lactic acid decreases the local pH feels like burn/fatigue

reverse lactic acid...occurs when

O2 supply catches up and Lactic Acid-->back to Pyruvate in a process known as the Cori Cycle..the amt of O2 necess to do this is the oxygen debt

why does cyanide kill us? DNP?

it blocks the final e- transfer to O2 whereas as DNP destroys mitochondria's ability to generate a useful H+ gradient for effective ATP generation

what does O2 do with the final e-?

it takes it from cyt a3 to make H20 (this is why we breathe to get O2 to our cells to pick up that e-!)

name 4 stages of gluc catabolism (aerobe)

glycolysis (cytoplasm)
pyruv decarb (mit mattic)
TCA cycle (mit matrix)
ETC (inner mit membrne)

what is created from the TCA cycle that we exhale?


the inner mitochondrial space is positive and acidic bc

free H+ accumulate in the mitochondrial matrix and are pumped into the intermembrane space accross the proton pump in a passive process "proton motive force"
-charged things can't permeate passively ..need channels

eukaryotic ATP production per glucose molecule

36 per molecule (whereas anerobe=2) so it's 18Xas effecient

Glycolysis ATP net in and out

2 ATP in -2 ATP
4 ATP out +4 (substrate)
2NADH (2ATP)/NADH +4 (oxidative)
net 6 ATP
(note that each NADH gives only 2 atp here bc its in cytopl.)

Pyruv Decarbox ATP net in and out

2 NADH (3ATP/NADH) +6 (oxidative)
net 6 ATP
(note each NADH gives 3 atp here because its not in cyto)

TCY cycle ATP net in and out

6NADH*(3atp/NADH) +18 ATP (oxidative)
2 FADH2 (2atp/FADH2) + 4ATP (oxidative)
2 ATP (1atp/GTP) +2 ATP (sub)
net 24

NADH in aerobic vs anaerobic

in aerobic: Glycolysis, Pyruv Decarb&TCA cycle, these reduced molecules are the products
in anaerobic: these are the reactants for Alcohola and Lactic Acid Fermentation whose products are oxidized to NAD+

FAD+ and FADH2 only in what step

only in the citric acid cycle and since its an aerobic process, this means it will be a FAD+input anda FADH2 product

carbohydrates come in

they are monosachs..
sugar polymers -->stored in liver 4 use later as GLYCOGEN
-glycogen is a polysach to make glucose 6 phosphate that can go to PGAL, pyruvate to eventual make acetyl coA and CO2 to go into the TCA cycle and event give off CO2

proteins come in

polypeps/amino acid (used when carbs insuff. )
removal of amine from acid by transaminases=B keto acids
converted to acetyl coA go to TCA cycle-CO2

lipids come in

fats=stored in adipose tissue as trigylcerides (triaglycerol)
esterifed to GLYCEROL 4 long term storage
real NRG stored in fatty acids go thru BETA OXID to create acetyl coA..give nadh and fadh2
can generate near 100 atp from 1 fat molecule (amazingly efficient energy storage)

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