Topic 2 - Cells Flashcards
(89 cards)
1
Q
What are the distinguishing features of eukaryotic cells
A
- Cytoplasm containing membrane-bound organelles
- DNA enclosed within the nucleus
2
Q
General structure of eukaryotic cells
A
Draw animal and plant cell
3
Q
Structure of cell surface membrane
A
- hydrophobic phosphate heads -> point to/attracted to water
- hydrophobic fatty acid tails -> point away/repelled from water
- proteins
- phospholipid bilayer
4
Q
Function of cell surface membrane
A
- Selectively permeable -> enables control of passage of substances in and out of cell
- Molecules/receptors/antigens on surface -> allows cell recognition/signalling
5
Q
Structure of nucleus
A
- Nuclear envelope -> double membrane and has nuclear pores
- Nucleoplasm -> granular jelly like substance
- Nucleolus -> dense region - site of RNA production and makes ribosomes
- Protein/histone bound linear DNA -> chromatin = condensed, chromosome = highly condensed
6
Q
Function of nucleus
A
- Holds/stores genetic information which codes for polypeptides (proteins)
- Site of DNA replication
- Site of transcription (part of protein synthesis) - producing mRNA
- Nucleolus makes ribosomes / rRNA
7
Q
Structure of ribosome
A
- Made of ribosomal RNA and protein -> 2 subunits
- Not membrane bound organelle
- 80s ribosomes are larger -> found in eukaryotes
- 70s ribosomes are smaller -> found in prokaryotes, mitochondria and chloroplasts
8
Q
Function of ribosome
A
-Site of protein synthesis (translation)
8
Q
Structure of rough (rER) & smooth endoplasmic reticulum (sER)
A
- rER have ribosomes on cisternae
- system of folded membranes called cisternae
9
Q
Function of rER & sER
A
- Rough endoplasmic reticulum
-> ribosomes on surface synthesize proteins
-> proteins are processed/folded/transported inside rER
-> proteins packaged into vesicles for transport (eg to golgi apparatus) - Smooth endoplasmic reticulum
-> synthesise and processes lipids
-> eg - cholesterol & steroid hormones
10
Q
Structure of golgi apparatus & golgi vesicles
A
- golgi apparatus-> flattened membrane sacs - folded membranes makes cisternae
- golgi vesicle -> small membrane sac - pinch off from cisternae
11
Q
Function of golgi apparatus & golgi vesicles
A
- Golgi apparatus
-> Modifies protein, eg. adds carbohydrates to produce glycoproteins
-> Modifies lipids, eg. adds carbohydrates to make glycolipids
-> Packages proteins / lipids into Golgi vesicles
-> Produces lysosomes (a type of Golgi vesicle) - Golgi vesicles
-> Transports proteins / lipids to their required destination - finished products transported to cell surface in golgi vesicles where they fuse with the membrane to release contents
12
Q
Structure of lysosomes
A
- membrane containing hydrolytic enzymes (lysozymes)
13
Q
Function of lysosomes
A
- Release hydrolytic enzymes (lysozymes)
- Which break down/hydrolyse pathogens or digest worn out cell components for reuse of materials
13
Q
Structure of mitochondria
A
- outer membrane
- cristae -> inner membrane fold
- matrix containing small ribosomes and circular DNA
14
Q
Function of mitochondria
A
- Site of aerobic respiration
- Produces ATP for energy release
- Eg - for protein synthesis/vesicle movement/active transport
15
Q
Structure of chloroplasts
A
- double membrane
- stroma containing -> thylakoid membrane (folded membrane embedded with pigment), 70s ribosomes, circular DNA, starch granules/lipid droplets
- lamella -> thylakoid linking grana
- grana -> stacks of thylakoid
15
Q
Function of chloroplasts
A
- Absorb light energy for photosynthesis
- To produce organic substances eg, carbohydrates and lipids
15
Q
Structure of cell wall in plants, algae, fungi
A
- Composed mainly of cellulose (polysaccharide) in plants/algae
- Composed of chitin (nitrogen containing polysaccharide) in fungi
15
Q
Function of cell wall in plants, algae, fungi
A
- Provide mechanical strength to cell - prevent cell bursting or changing shape under osmotic pressure
16
Q
Structure of cell vacuole in plants
A
- cell sap surrounded by single membrane called tonoplast membrane
16
Q
Function of cell vacuole in plants
A
- Maintain turgor pressure in cell (stop plant from wilting) to provide support
- Contains cell sap -> stores sugars, amino acids, pigments and waste chemicals
- pigments may colour petals to attract pollinators
16
Q
How are eukaryotic cells organised in complex multicellular organisms
A
- Tissue -> group of specialised cells with similar structure working together to perform a specific function - often with the same origin
- Organ -> aggregations of tissues performing specific functions
- Organ system -> group of organs working together to perform specific functions
16
Q
What are distinguishing features of prokaryotic cells
A
- Cytoplasm lacking membrane bound organelles
- Genetic material is not enclosed in a nucleus
16
General structure of prokaryotic cells
- Capsule (slimly layer made of protein that prevents bacteria from drying out and protects the bacteria against the hosts immune system), plasmids (small rings of DNA), flagella (rotates to allow bacteria to move) are SOMETIMES present
- Cell surface membrane, cell wall (containing murein glycoprotein), cytoplasm, small ribosomes, circular DNA are ALWAYS present
16
Compare structure of eukaryotic and prokaryotic cells
- Eukaryotic has membrane bound organelles - prokaryotic does not
- Eukaryotic has nucleus - prokaryotic does not
- Eukaryotic DNA is long and linear & associated with histone proteins - prokaryotic DNA is short and circulator and isn't associated with proteins
- Eukaryotic has larger(80s) ribosomes - prokaryotic has smaller (70s) ribosomes
- Cell wall is only present in plants,algae and fungi (made of cellulose/chitin) - prokaryotic cell wall is present in all cells (made of murein)
16
Why are viruses acellular and non living
- Acellular -> not made of cells, no cell membrane/cytoplasm/organelles
- Non living -> no metabolism - cant independently move/respire/replicate
16
General structure of virus
- Nucleic acids surrounded by capsid (protein coat)
- Attachment proteins allow attachment to specific host cells
- No cytoplasm, ribosomes,cell wall, cell membrane etc
- Some are surrounded by lipid envelope (HIV)
16
What is magnification and resolution
- Magnification = number of times greater image is than size of real object
(size of image/size of actual object)
- Resolution = minimum distance between 2 points to be distinguished as 2 separate points
16
Optical microscopes
- Light is focused using glass lenses
- Light passes through specimen -> different structures absorb different amounts & wavelengths
- 2D image of cross section
- Low resolution due to long wavelength of light
- Cant see internal structure of organelles or ribosomes
- Thin specimen
- Low magnification (X1500)
- Can view living organisms
Simple preparation
- Can view in colour
17
Transmission electron microscope (TEM)
- Electrons focused using electromagnets
- Electrons pass through specimen -> denser parts absorb more and appear darker
- 2D image of cross section
- Very high resolution due to short wavelength of electrons
- Can see internal structures of organelles and ribosomes
- Very thin specimen
- High magnification (X1,000,000)
- Can only view dead specimens -> uses vacuum
- Complex preparation so artefacts are often present
- Can't view in colour
17
Scanning electron microscope (SEM)
- Electrons focused using electromagnets
- Electrons are deflected/bounce off specimen surface
- 3D image of surface
- High resolution due to short wavelength of electrons
- Cant see internal structures
- Specimen doesn't have to be thin
- High magnification (X1,000,000)
- Can only view dead specimens -> uses vacuum
- Complex preparation so artefacts are often present
- Can't view in colour
17
How do scientists distinguish between artefacts (dust, air bubbles) and cell organelles
- Scientists prepare specimens in different ways
- If object seen with one technique but not another -> more likely to be an artefact
17
How to calculate magnification
- image size = actual size x magnification
17
Converting between units
metre x1000 -> millimetre x1000> micrometre x1000 -> nanometre
17
Describe how the size of an object viewed with an optical microscope can be measured
1 - line up eyepiece graticule with stage micrometre
2 - calibrate eyepiece graticule -> use stage micrometre to calculate increments on eyepiece graticule
3 - take micrometre away - use graticule to measure how many divisions make up object
4 - calculate size of object by multiplying number of divisions by size of division
5 - recalibrate eyepiece graticule at different magnifications
17
Cell fractionation & ultracentrifugation to separate cell components
1 - homogenise tissue/use blender - disrupts cell membrane - breaks open cell to release contents/organelles
2 - place in cold, isotonic, buffered solution - cold to reduce enzyme activity so that organelles not broken down - isotonic so water doesn't move in or out of organelles by osmosis so they don't burst - buffered to keep pH constant so enzymes don't denature
3 - filter homogenate - remove large, unwanted debris (whole cells or connective tissue)
4 - ultracentrifugation (separates organelles in order of mass) - centrifuge homogenate in tube at low speed - remove pellet of heaviest organelle and respin supernatant at higher speed - repeat at increasing speeds until separated - each time the pellet is made of lighter organelles (nucleus -> chloroplasts -> mitochondria etc)
17
Summarise stages of cell cycle in eukaryotic cells
- Stage 1 - Interphase -> DNA replicates semi-conservatively (S phase) - leads to 2 chromatids (identical copies) joined at centromere - number of organelles & volume of cytoplasm increases, protein synthesis (G1/G2)
- Stage 2 - Mitosis -> nucleus divides, produces 2 nuclei with identical copies of DNA produced by parent cell
- Stage 3 - Cytokinesis -> cytoplasm and cell membrane (normally) divide - forms 2 new genetically identical daughter cells
17
Stages of mitosis
- Stage 1 - Prophase
-> chromosomes condense, become shorter/thicker so are visible - appear as 2 sister chromatids joined at a centromere
-> nuclear envelope breaks down
-> centrioles move to opposite poles forming spindle network
-> spindle fibres start to attach to chromosomes by centromeres
- Stage 2 - Metaphase
-> spindle fibres attach to chromosomes by their centromeres
-> chromosomes align along equator
- Stage 3 - Anaphase
-> spindle fibres shorten/contract
-> centromere divides
-> pulls chromatids (from each pair) to opposite ends of cell
- Stage 4 - Telophase
-> chromosomes uncoil, become longer/thinner
-> nuclear envelope reform = 2 nuclei
-> spindle fibres/centrioles break down
17
Why do some eukaryotic cells not undergo cell cycle
- Within multicellular organisms, not all cells retain ability to divide
- Only cells that do retain this ability can go through a cell cycle
17
Importance of mitosis in life of an organism
- Parent cell divides to produce 2 genetically identical daughter cells for
-> growth of multicellular organisms by increasing cell number
-> replacing cells to repair damaged tissues
-> asexual reproduction
17
Describe how tumours & cancers form
Mitosis is a controlled process so
-> mutations in DNA/genes controlling mitosis can lead to uncontrolled cell division
-> tumours form if this results in mass of abnormal cells
- malignant tumour = cancerous and can spread by metastasis
- benign tumour = non cancerous
17
How do cancer treatments control cell division rate
Some disrupt spindle fibre activity/formation
-> chromosomes can’t attach to spindle by their centromere
-> chromatids can’t be separated to opposite poles (no anaphase)
-> prevents/slows down mitosis
Some prevent DNA replication in interphase
-> can’t make 2 copies of each chromosome
-> prevents/slows down mitosis
18
How do prokaryotic cells replicate (binary fission)
- Replication of circular DNA
- Replication of plasmids
- Division of cytoplasm to produce 2 daughter cells - single copy of circular DNA - variable number of copies of plasmids
18
How do viruses replicate
- Non living so don’t go through cell division
- Attachment proteins attach to complementary receptors on host cell
- Inject viral nucleic acid into host cell
- Infected host cell replicates virus particles
-> nucleic acid replicated - cell produces viral protein/capsid/enzymes - virus is assembled then released
18
Describe fluid mosaic model of membrane structure
- Molecules are free to move laterally in phospholipid bilayer
- Many components -> phospholipids, proteins, glycoproteins, glycolipids
18
Describe arrangement of components of cell membrane
- Phospholipids form bilayer -> fatty acid tails face inwards - phosphate heads face outwards
- Proteins -> intrinsic proteins span bilayer (channel/carrier) - extrinsic proteins on surface of membrane
- Glycolipids (lipids with polysaccharide chains attached) - found on exterior surface
- Glycoproteins (proteins with polysaccharide chains attached) - found on exterior surface
- Cholesterol (sometimes present) - bonds to phospholipid hydrophobic fatty acid tails
18
Arrangement of phospholipids in cell membrane
- Bilayer - water present on either side
- Hydrophobic fatty acid tails repel from water so point towards interior
- Hydrophilic phosphate heads attracted to water so point to water
18
Role of cholesterol in cell membranes
- Restricts movement of other molecules making up membrane
- Decreases fluidity and permeability/ increases rigidity
18
How are cell membranes adapted to functions
- Phospholipid bilayer is fluid -> membrane can bend for vesicle formation/phagocytosis
- Glycoproteins/glycolipids -> act as receptors/antigens - involved in cell signalling and recognition
18
How does movement across membrane occur by simple diffusion
- Lipid soluble (non polar) or very small substances
- Move from area of higher concentration to area of lower concentration down a concentration gradient
- Across phospholipid bilayer
- Passive - doesn’t require energy from ATP/respiration
18
Limitations imposed by phospholipid bilayer
- Restricts movement of water soluble (polar) & larger substances
- Due to hydrophobic fatty acid tails in interior of bilayer
18
How does movement across membrane occur by facilitated diffusion
- Water soluble/polar/charged or slightly larger substances
- Move down concentration gradient
- Through specific channel/carrier proteins
- Passive - doesn’t require energy from ATP/respiration
19
How does movement across membrane occur by osmosis
- Water diffuses/moves
- From area of high to low water potential - down a water potential gradient
- Through partially permeable membrane
- Passive - doesn’t require energy from ATP/respiration
19
How does movement across membrane occur by active transport
- Substances move from area of lower to higher concentration
- Against concentration gradient
- Requires hydrolysis of ATP and specific carrier proteins
19
Describe role of carrier proteins and importance of hydrolysis of ATP in active transport
1 - complementary substance binds to specific carrier proteins
2 - ATP binds - hydrolysed into ADP + Pi - releases energy
3 - carrier protein changes shape - releases substance on side of higher concentration
4 - Pi released - protein returns to original shape
19
How does movement across membrane occur by co-transport
- Two different substances bind and move simultaneously by a co-transporter protein
- Movement of one substance against its concentration gradient is coupled with movement of another substance down its concentration gradient
19
Example of co-transport - absorption of sodium ions and glucose
- Sodium ions are actively transported from epithelial cells to blood by sodium potassium pump
- Establishes concentration gradient of sodium (higher in lumen than epithelial cell)
- Sodium ions enter epithelial cells down concentration gradient with glucose against its concentration gradient - by a cotransporter protein
- Glucose moves down concentration gradient into blood by facilitated diffusion
- Movement of sodium is considered indirect/secondary active transport as it is reliant on a concentration gradient created by active transport
19
How surface area, number of channel or carrier proteins and differences in gradients of concentration or water potential affect the rate of movement across cell membranes
- Increasing surface area of membrane -> increases rate of movement
- Increasing number of channel/carrier proteins increases rate of facilitated diffusion/active transport
- Increasing concentration gradient increases rate of simple diffusion
Increasing concentration gradient increases rate of facilitated diffusion
-> until number of channel/carrier proteins becomes a limiting factor as they are all in use
- Increasing water potential gradient increases rate of osmosis
19
Adaptations of specialised cells in relation to rate of transport across internal/external membranes
- Cell membrane is folded (microvilli in ileum) - increases surface area
- More protein channels/carriers -> for facilitated diffusion (active transport - carrier proteins only)
- Large number of mitochondria -> makes more ATP by aerobic respiration for active transport
19
What is an antigen
- Foreign molecule /protein /glycoprotein/ glycolipid
- Stimulates immune response leading to antibody production
19
How are cells identified by immune system
- Each type of cell has specific molecules on its surface (cell wall/membrane) which identify it
- These are often proteins -> which have a specific tertiary structure (or glycolipids/glycoproteins)
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What types of cells and molecules can the immune system identify
1 - pathogens (disease causing microorganisms) - viruses, fungi, bacteria
2 - cells from other organisms of the same species (organ transplants)
3 - abnormal body cells - eg, tumour cells or virus infected cells
4 - toxins (poisons) released by some bacteria
19
Phagocytosis of pathogens - non specific immune response
1 - phagocyte is attracted by chemicals released by the pathogen - recognises foreign antigens on pathogen
2 - phagocyte engulfs pathogen by surrounding it with its cell membrane
3 - pathogen contained in vesicle/phagosome in cytoplasm of phagocyte
4 - lysosome fuses with phagosome and releases lysozymes (hydrolytic enzymes)
5 - lysozymes hydrolyse/digest pathogens
Phagocytosis leads to antigens being presented/displayed on the phagocyte cell surface membrane -> stimulates specific immune response (cellular & humoral)
19
Response of T lymphocytes to foreign antigens (cellular response)
- T lymphocytes recognise antigens on surface of antigen presenting cells (infected cells, phagocytes presenting antigens, tumour cells etc)
- Specific T helper cells with complementary receptors bind to antigen on antigen presenting cells -> these become activated and divide by mitosis which stimulates
-> Cytotoxic T cells - kill infected cells/tumour cells - produce perforin
-> Specific B cells -> humoral response
-> Phagocytes -> engulf pathogens by phagocytosis
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Response of B lymphocytes to foreign antigens - humoral response
- B lymphocytes recognise free antigens in the blood/tissues - not just antigen presenting cells
-Specific B lymphocytes with complementary receptors (antibody on cell surface) binds to antigen
- Stimulated by helper T cells - release cytokines
- Divides rapidly by mitosis to form clones
- Some differentiate into B plasma cells -> secrete large amounts of monoclonal antibodies
- Some differentiate into B memory cells -> remain in blood for secondary immune response
20
What are antibodies
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Structure of antibody
- Y shaped ->heavy and light polypeptide chain, hinge region, variable region, antigen binding site, disulfide bridge
20
How do antibodies lead to pathogen destruction
- Antibodies bind to antigens on pathogens forming antigen-antibody complexes
-> specific tertiary structure so binding site/variable region binds to complementary antigen
- Each antibody can bind to 2 pathogens at a time -> agglutination of pathogens
- Antibodies attract phagocytes
- Phagocytes bind to antibodies and phagocytose many pathogens at once
20
Difference between primary and secondary immune response
- Primary (first exposure to antigen)
-> antibodies are produced slowly at a low concentration
-> takes time for specific B plasma cells to be stimulated to produce specific antibodies
-> produces memory cells
- Secondary (second exposure to antigen)
-> antibodies produced faster at a higher concentration
-> B memory cells rapidly undergo mitosis to produce many plasma cells which produce specific antibodies
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What is a vaccine
- Injection of antigens from attenuated (dead/weakened) pathogens - stimulates formation of memory cells
20
How do vaccines provide protection for individuals against disease
1 - specific B lymphocytes with complementary receptors bind to antigen
2 - specific T helper cells bind to APC and stimulates B cell
3 - B lymphocytes divide by mitosis to form clones
4 - some differentiate into B plasma cells which release antibodies
5 - some differentiate into B memory cells
6 - on secondary exposure to antigen, B memory cells rapidly divide by mitosis to
produce B plasma cells - releases antibodies faster at a higher concentration
20
How do vaccines provide protection for populations against disease
- Herd immunity -> large proportion of population is vaccinated - reduces spread of pathogen
- large proportion of population is immune so don’t become ill from infection
- fewer infected people to pass pathogen on/unvaccinated people are less likely to come in contact with someone with disease
20
Describe differences between active (AI) & passive immunity (PI)
-AI has initial exposure to antigen (vaccine or primary infection) but PI has no exposure to antigen
- AI involves memory cells but PI does not
- AI produces antibodies secreted by B plasma cells but PI antibodies are introduced from another organism
- AI is slow and takes long to develop but PI is faster acting
- AI provides long term immunity as antibody can be produced in response to a specific antigen again but PI provides short term immunity as antibody is hydrolysed (endo/exo/dipeptidases)
20
Effect of antigen variability on disease and disease prevention
- Antigens on pathogens change shape/tertiary structure due to gene mutations (creates new strains)
- No longer immune from vaccine or prior infection
-> B memory cell receptors cannot bind or recognise the changed antigens on secondary exposure
-> specific antibodies are not complementary and cannot bind to changed antigen
21
Structure of HIV particle
- lipid envelope, RNA, reverse transcriptase, capsid, attachment proteins
21
Replication of HIV in helper T cells
1 - HIV attachment proteins attach to receptors on helper T cells
2 - Lipid envelope fuses with cell surface membrane -> releases capsid into cell
3 - Capsid uncoating, releases RNA and reverse transcriptase
4 - Reverse transcriptase converts viral RNA to DNA
5 - Viral DNA is inserted/incorporated into helper T cell DNA (can remain latent)
6 - Viral protein/capsid/enzymes are produced
-> DNA transcribed into HIV mRNA
-> HIV mRNA translated into new HIV proteins
7 - Virus particles assembled and released from cells by budding
21
How does HIV cause symptoms of acquired immune deficiency syndromes (AIDS)
- HIV infects and kills helper T cells (host cell) as it multiplies rapidly
-> T helper cells cannot stimulate cytotoxic T cells, B cells and phagocytes
-> so B plasma cells cannot release as many antibodies for agglutination and destruction of pathogens
- Immune system deteriorates -> becomes more susceptible to opportunistic infections
- Pathogens reproduce, release toxins and damage cells
22
Explain why antibiotics are ineffective against viruses
- Viruses do not have structures/processes that antibiotics inhibit
- Viruses do not have metabolic processes (don’t make proteins)/ribosomes
- Viruses do not have bacterial enzymes/murein cell wall
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What is a monoclonal antibody
- Antibody procured from genetically identical/cloned B lymphocytes/plasma cells
- Have same tertiary structure
22
How are monoclonal antibodies used in medical treatments
- Monoclonal antibody has specific tertiary structure/binding site/variable region
- Complementary to receptor/protein/antigen found only on specific cell type (eg cancer cell)
- Therapeutic drug attached to antibody
- Antibody binds to specific cell - forms antigen-antibody complex - delivers drug
- Some mABs are also designed to block antigens/receptors on cells
22
How are monoclonal antibodies used in medical diagnosis
- Monoclonal antibody has specific tertiary structure/binding site/variable region
- Complementary to specific receptor/protein/antigen associated to diagnosis
- Dye/stain/fluorescent marker attached to antibody
- Antibody binds to receptor/protein/antigen - forms antigen-antibody complex
23
General ethical issues associated with use of vaccines and monoclonal antibodies
- Preclinical testing on animals -> potential stress/harm/mistreatment -> BUT animals not killed and helps produce new drugs to reduce human suffering
- Clinical trials on humans -> potential harm and side effects
- Vaccines -> may continue high risk activities and still develop/pass pathogen
- Use of drugs -> potentially dangerous side effects
23
Points to consider when evaluating methodology relating to the use of vaccines and monoclonal antibodies
- Was the sample size large enough to be representative?
- Were participants diverse in terms of age, sex, ethnicity and health status?
- Were placebo / control groups used for comparison?
- Was the duration of the study long enough to show long-term effects?
- Was the trial double-blind (neither doctor / patient knew who was given drug or placebo) to reduce bias?
23
Points to consider when evaluating evidence and data relating to the use of vaccines and monoclonal antibodies
- What side effects were observed, and how frequently did they occur?
- Was a statistical test used to see if there was a significant difference between start & final results?
- Was the standard deviation of final results large, showing some people did not benefit?
- Did standard deviations of start & final results overlap, showing there may not be a significant difference?
- What dosage was optimum? Does increasing dose increase effectiveness enough to justify extra cost?
- Was the cost of production & distribution low enough?
24
Use of antibodies in the ELISA (enzyme-linked immunosorbent assay) test to detect antigens
Method 1 - DIRECT ELISA
- Attach sample with potential antigens to well
- Add complementary monoclonal antibodies with enzymes attached -> bind to antigens if present
- Wash well -> removes unbound antibodies to prevent false positive
- Add substrate -> enzymes create products that cause a colour change (positive result)
Method 2 - SANDWICH ELISA
- Attach specific monoclonal antibodies to well
- Add sample with potential antigens, then wash well
- Add complementary monoclonal antibodies with enzymes attached -> bind to antigens if present
- Wash well -> removes unbound antibodies to prevent false positive
- Add substrate -> enzymes create products that cause a colour change
25
Use of antibodies in the ELISA test to detect antibodies
Method - INDIRECT ELISA
- Attach specific antigens to well
- Add sample with potential antibodies, wash well
- Add complementary monoclonal antibodies with enzymes attached -> bind to antibodies if present
- Wash well -> remove unbound antibodies
- Add substrate -> enzymes create products that cause a colour change
25
Purpose of control well in ELISA test
- Compare to test to show only enzyme causes the colour change
- Compare to test to show all unbound antibodies have been washed away
25
Why does failure to thoroughly wash the well result in false positives
- Antibody with enzyme remains - not washed out
- So substrate converted into colour product
