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Grading

Excellent / Thorough piece of work.
Excellent knowledge, understanding and application of AS & A2 knowledge.
Good / Most parts completed to a high standard, but there are still some areas you need to work on.
Few, if any, questions left unanswered.
Satisfactory / Good in parts, but a significant number of answers require improvement, and/or several questions were not attempted
Unsatisfactory / Not enough effort put into the booklet.
Too many gaps and/or not enough detail in most questions. Gives the impression of being rushed, or not thought out properly.


Revision pack 1

Why mint?

All mint plants belong to the genus Mentha, There are 18 recognised species of Mentha, with numerous varieties and a further 11 hybrids (created by crossing two different species). They grow in the wild on every continent except Antarctica, and are noted for their production on essential oils. They have been used traditionally for more than 2000 years as a source of medical remedies, flavourings, fragrances and even as a source of insecticides.

Mint plants are currently one of the most important commercial herbs grown, as the essential oils they produce are of high economic value. The most important commercial mint species are Mentha x piperita (peppermint), Mentha spicata (Native spearmint), Mentha x gracilis (Scotch spearmint) and Mentha canadensis (cornmint). Both Native and Scotch Spearmint are mainly produced in North America and China; peppermint oil is produced in the USA and India, while cornmint oil is mainly produced in India. Globally, over 40,000 tonnes of mint oils are produced per annum, with a value of over $800 million.

The essential oils produced by different mint plants are a complex mix of alcohols, monoterpenes and other hydrocarbons, oxides, esters, aldehydes and ketones and to a lesser extent carboxylic acids. Peppermint oil is mainly composed of L-L-menthol and L-menthone; cornmint oil is mainly composed of L-menthol and spearmint oil is mainly composed of L-carvone.

Other important mint oils include pennyroyal oil (an oil rich in the ketone D-pulegone), produced by Mentha pulegium, and bergamot oil, produced by Mentha aquatic var. citrata oil, which is rich in linalool and linalyl acetate.

The essential oils produced by mint plants are secreted by specialised cells and stored in circular structures called trichomes. These are small glandular outgrowths of the leaf epidermis. The natural role of these oils is to inhibit the growth of other competitor plant species (allelopathy), and to protect the mint plants from attack by insects and pathogens such as bacteria and fungi.

Wrigley’s peppermint flavoured chewing gum was first

marketed in 1893, in the same year that Colgate

introduced mint-flavoured toothpaste.

Find out more about the historical and commercial uses of mint plants and the essential oils they produce. Place your summary here – in any form that suits you (e.g. written; pictorial).

Consider food and drink, fragrances, medicines and any other uses you can find. (10 marks)

Mint hint: do an internet search using key words on page 1 to help you.

There are plenty of mint sources out there!

* Food & Drink:

- mint tea.

- mint sauce.

- mint jelly.

- mint chocolate.

- mint sweets.

- crème de menthe.

- mint lemonade.

- chewing gum.

- as a preservative.

* Fragrances:

- aromatherapy oils.

- soaps, bath oils, shampoo, shower gel.

- air freshener.

- cosmetics.

* Medicines:

- cough remedies.

- decongestants.

- treatment of insect bites.

- indigestion remedies.

- treatment of IBS.

- antiseptics.

* Other:

- insecticides.

- menthol cigarettes.

- mouth wash.

- breath freshener.


Cell Membranes (AS-1.1.2)

Biological Molecules (AS-2.1.1)

Have you ever wondered why mints make your mouth feel cold? In common with many other parts of your body, your mouth contains sensory receptor cells called thermoreceptors. The cell surface membrane of these cells contains a protein ion channel called theTransient receptor potential cation channel subfamily M member 8, or TRPM8. This channel opens in the presence of cold temperature, possibly because changes in temperature cause the receptor to change shape, allowing Na+ ions into the cell. The resulting depolarisation leads to the transmission of a nerve impulse to the thermoregulatory centre in brain, which interprets the impulse as a cold sensation.

Researchers have found that L-L-menthol, an organic compound found in a few mint oils, activates the same receptor by causing it to change shape, leading to the “cold” sensation we feel when tasting mint. What’s more, if you suck on a mint and drink cold water at the same time, the “double dose” of sensory information causes an extra cold sensation. Try it!

Source: http://boundlessthicket.blogspot.co.uk/2012/04/that-cool-mint-feeling-when-i-was-in.html

(which includes research citations).

Suggest why Na+ ions enter cells through protein channels in the cell membrane rather than directly through the phospholipid bilayer. (1 mark)

* Charged ions cannot penetrate phospholipid bilayer easily (as it is non-polar).

Suggest how L-menthol changes TRPM8 channel’s shape, with reference to changes inTRPM8’s tertiary structure. (2 marks)

* Binds to the protein.

*Altering bonds holding together its 3D shape.


Nerves (A2-4.1.2)

Describe how influx of Na+ ions into a sensory receptor sets up an action potential, with reference to generator potentials and the “all-or-nothing” response. (5 marks)

* Stimulus causes non-voltage gated sodium channels to open in receptor cells.

* Na+ ions diffuse into the receptor cell and cause it to depolarise.

* Generator potential is set up (small positive charge across the membrane).

* If enough non-voltage gated sodium channels open, threshold potential (-50mV) is reached.

* Once this threshold potential is reached, nearby voltage-gated sodium channels open.

* This sets off an action potential in the receptor cells, transmitted as a nerve impulse.

* This is a all-or-nothing response: the stimulus either sets off an

action potential (+40 mV) or it doesn’t.

Outline how an action potential is transmitted along a neurone. (4 marks)

* Increase in Na+ ion conc. in the sensory receptor sets up a local current of Na+ ions.

* Na+ ions diffuse sideways along the inside of neurone away from the region of higher conc.

* This causes voltage-gated sodium channels to open further down the neurone, setting off another action potential.

* The local current moves down the neurone as a wave of depolarisation (followed by a wave of repolarisation) – this is the nerve impulse.

Why do myelinated neurones transmit action potentials faster than unmyelinated? (3 marks)

* Myelin is impermeable to Na+ and K+ ions.

* Myelin provides electrical insulation.

* In myelinated neurones, depolarisation occurs only at the gaps in the myelin sheath.

* Called the nodes of Ranvier.

* So action potentials jumps from node to node (saltatory conduction).

Name the type of neurone which transmits action potentials from the sensory receptor to the brain. (1 mark)

* Sensory neurone.

Describe two distinguishing features of this type of neurone. (2 marks)

* Short axon.

* Long dendron.

* Cell body along one side / outside the CNS / in the dorsal root ganglion.

Communication (A2-4.1.1)

Mice which lack the gene that codes for the TRMP8 receptor are called TRMP8-null mutants. Three independent research groups have reported that these mutants are severely impaired in their ability to detect cold temperatures.

Suggest how and why the inability of TRT8-null mutant mice to detect cold could lead to death of these mice in a cold environment. Include reference to the following in your answer:

*homeostasis (1 mark)

*endotherms (2 marks)

*thermoreceptors (2 marks)

*how mice normally thermoregulate in the cold (3 marks)

*whyTRT8-null mutant mice die in the cold (2 marks)

* Homeostasis is maintenance of a constant internal environment.

* Endotherms are organisms that can use internal sources of heat to regulate body temp.

* Endotherms keep a constant core temp.(temp. of blood flowing through the brain & vital organs) at an optimum for enzyme activity.

* Thermorecepors are normally responsible for detecting changes in the core temp. of blood running through the hypothalamus.

* Thermoreceptors also monitor changes in skin temp. to detect changes in external temp.

* The thermoregulatory centre in the hypothalamus processes the input from thermoreceptors to bring about physiological ad behavioural responses which help maintain core temperature.

* Normal thermoregulation: if core temperature falls too low, responses include mechanisms to increase heat production and to reduce heat loss.

* These include:

-contraction of erector pili muscles (hairs on skin raise to trap a layer of insulating air).

-vasoconstriction of arterioles in the skin, to reduce heat loss by radiation.

-increased rate of metabolism to generate more heat, especially in the liver.

-behavioural responses to reduce heat loss, e.g. huddling, seeking sun or seeking shelter.

* ForTRT8-null mutant mice, failure to detect falling environmental temp. and falling core body temp. will lead to failure of mechanisms to increase heat production/decrease heat loss.

* Leads to hypothermia /death.

Hormones (A2-4.1.3)

Diabetes mellitus is a serious metabolic disorder associated with hyperglycaemia (high blood glucose concentration). To investigate claims that herbal (plant) remedies can reduce blood glucose concentration in diabetics, researchers from the University of Madras in India carried out experiments to study the efficacy (effectiveness) of extracts of four types of plant on the concentration of blood glucose, blood insulin, liver enzyme and liver glycogen levels in diabetic rats.

All four plants are used on Indian cooking, have religious significance and have a history of medicinal use in India. One of the plants tested was Mentha x piperita (peppermint).

For the investigation, male albino rats of the Wistar strain were used. Some rats were treated with the drug streptozotocin to induce diabetes, and some rats were left untreated (normal). Rats were divided into six groups, each group containing at least six rats:

Group I Normal rats (normal control group)

Group II Diabetic rats (diabetic control group).

Group III Diabetic rats fed with Murraya koenigii (curry leaf tree)

Group IV Diabetic rats fed with Aegle marmelos (Bengal quince)

Group V Diabetic rats fed with Ocimum sanctum (Holy Basil)

Group VI Diabetic rats fed with Mentha x piperita

Treated rats were fed daily with plant extracts for 29 days.

On the 29th day, they were fasted, then fed a fixed amount of glucose. The changes in blood glucose concentration (BGC) over the next 2 hours were measure every 30 minutes (glucose tolerance test – Table 1).

On the 30th day, the rats were fasted again, and then killed.

Various assays were done to measure the concentration of glycogen and enzymes in the rats’ livers and glucose and insulin in the rats’ blood, amongst other things. The results for groups I, II and VI will be considered here to ascertain the effect of oral peppermint extract.

Source: R. T. Narendhirakannan et al., “Biochemical evaluation of antidiabetogenic properties of some commonly used Indian plants on streptozotocin-induced diabetes in experimental rats,”Clinical & Experimental Pharmacology & Physiology, vol 33, no 12, pp 1150–1157, 2006

Graph 1 Average fasting blood glucose concentration (BGC) in normal rats (Group I), untreated diabetic rats (Group II) and diabetic rats treated with plant extracts for 30 days (Groups III to VI).

Which plant extract is the most effective at reducing fasting BGC? (see key). (1 mark)

* Murraya koenigii (curry leaf tree).

Table 1: Glucose tolerance test: changes in blood glucose concentration (BGC) in normal, untreated diabetic and peppermint-treated diabetic rats after 30 days of treatment, at 30 minute intervals following ingestion of 2g/kg glucose.

Rat Group / Mean Blood Glucose Concentration (BGC) (mg/dL)
Fasting / 30 min / 60 min / 90 min / 120 min
(I) Normal control / 79.5 / 149.6 / 168.0 / 128.6 / 87.4
(II) Diabetic control / 252.4 / 319.4 / 359.4 / 336.5 / 311.4
(VI) Diabetic + peppermint treatment / 135.7 / 178.8 / 215.5 / 201.8 / 143.8

(a) Calculate % difference in fasting BGC in group (II) diabetic control rats versus

group (I) normal control rats. (2 marks)

* 252.4 – 79.5 X 100 = 217.5 % higher in diabetic control.

79.5

OR 252.4 – 79.5 X 100 = 68.5 % lower in normal control

252.4

(b) Calculate % decrease in fasting BGC in group (VI) diabetic + peppermint rats versus

group (II) diabetic control rats. (2 marks)

* 252.4 – 135.7 X 100 = 46.2 % decrease.

252.4

(c) At what time does mean BGC peak in all three rat groups? (1 mark) * 60 minutes.

(d) Explain why mean BCG takes time to peak, following glucose ingestion. (1 mark)

* Takes time to absorb glucose from gut/small intestine into the blood capillaries.


Hormones (A2-4.1.3)

Draw a flow diagram to outline how an increase in BGC leads to increased insulin secretion in normal rats. (5 marks)

* Increased BGC à more glucose diffuses into β-cells through channel proteins.

* Glucose is used to make ATP in respiration.

* ATP closes the K+ channels.

* K+ ions accumulate in β-cells, so they depolarise.

* Voltage-gated Ca2+ gates open, so Ca2+ ions diffuse into the β-cells.

* Vesicles containing insulin migrate to plasma membrane of β-cells and fuse.

* Insulin released by exocytosis.

Figure 3 shows some of the reactions involved in the processing of glucose by hepatocytes:

Fill in the names of the missing processes in the correct boxes: (3 marks)

gluconeogenesis glycogenolysis glycogenesis

Name the process stimulated by insulin: (1 mark)

* glycogenesis.

Name two hormones which increase blood glucose: (2 mark)

* glucagon. * adrenaline.


Table 2: Mean glycogen, enzyme and insulin levels in normal, untreated diabetic

and peppermint-treated diabetic rats after 30 days of treatment

Concentration measured / Group I
(normal control) / Group II
(diabetic control: untreated) / Group VI
(diabetic: peppermint treated)
Insulin in blood plasma (µmol/mL) / 16.6 / 4.3 / 7.4
Glycogen synthase in liver (µmol/mg) / 816.5 / 561.8 / 784.4
Glycogen phosphorylase in liver (µmol/mg) / 637.2 / 876.5 / 716.5
Glycogen in liver (mg/g) / 52.8 / 23.7 / 37.7

(a) Explain whether the diabetic rats have Type 1 or Type 2 diabetes. (2 marks)