BIOL 1010 Lecture Notes - Lysozyme, Lysosome, Turnover Number

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3 Feb 2014

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An introduction to metabolism: metabolism, energy and life. Metabolism is all of an organism"s chemical reactions (an emergent property that arises from. Metabolism interactions of molecules in the orderly environment of the cell: metabolism is very important for the management of cellular material and energy resources. 1* metabolic reactions are organized into pathways of enzyme controlled chemical reactions. Enzymes are required to make the reactions occur at a rate fast enough to support life. 2* cells need a supply of molecules (food) and energy. 3* cells need to get rid of waste products. 4* metabolic pathways begin with a specific molecule(s) and end with a product: catabolic pathways: 5* break down complex molecules into simple molecules. 6* energy stored in complex molecules is made available to do work or transformed into readily usable chemical forms (i. e. , atp) 7* small molecules resulting from the catabolism of complex energy rich molecules may be used by the cell to build new molecules.

Related Questions

1.When something appears blue, it is absorbing all colors except__________.

yellow

blue

red

green

orange

2.During heavy exercise, lactic acid can build up in ourmuscles. Why? How does this resemble the metabolism of bacteria andyeast?

lactic acid is results from insufficient oxygen during sugarmetabolism; it is fermentation

lactic acid accumulates when we are dehydrated; bacteria andyeast use the same pathway

lactic acid is built up from carbon dioxide; bacteria and yeaststore energy in this way

3.Why must a cell keep a similar concentration of dissolvedsubstances with the fluid surrounding them?

to avoid dilution of potential energy

to avoid osmotic imbalance and rapid gain or loss of water

to maintain the correct amount of dehydration and hydrolysis

4.What is entropy?

the amount of energy in a system

the amount of disorganization

the amount of organization

5.Burning a log is the reverse reaction found in photosynthesis.What products would be formed in burning a log?

carbon dioxide and water

glucose and oxygen

oxygen and carbon dioxide

oxygen and water

6.The main reason that cellular respiration needs to occur stepby step instead of a single, big reaction is

cells don't store enough oxygen

too much energy would be released for the cell to harness

cells don't have many mitochondria.

cells produce the enzymes needed for cellular respiration veryslowly

7.Enzymes are catalysts because they operate to:

raise activation energy

lower activation energy

supply activation energy

supply the reactants

8.When ATP powers a reaction it becomes ADP. The ADP

can reform ATP by an exergonic reaction

is a waste product for lysosomal breakdown

can reform ATP by an endergonic reaction

can reform ATP by an oxidation reaction

can reform ATP by an equilibrium reaction

9.The energy source that drives photosynthesis is

water

glucose

carbon dioxide

oxygen

sunlight

10. What is the process by which enzymes regulate their ownactivity?

osmosis

self-propulsion

feedback inhibition

11.Coupled reactions are reactions in which a

endergonic reaction drives a spontaneous reaction

exergonic reaction drives a spontaneous reaction

endergonic reaction drives an exergonic reaction

exergonic reaction drives an endergonic reaction

12.How is water used in photosynthesis?

as a substrate for ATP synthase

as an electron donor

to combine with ADP forming ATP

as an electron acceptor

13.Why are the âDark Reactionsâ of photosynthesis referred to asâDarkâ?

they do not require light

they can only occur at night

they generate excess sugar and the leaves turn brown

14.What is the difference between potential and kineticenergy?

potential is stored, kinetic is being used

potential is being used, kinetic is ready to be used

potential is negative, kinetic is positive

15.The products of cellular respiration are

carbon dioxide, water, and ATP

glucose, water, and ATP

glucose, carbon dioxide, and ATP

oxygen, ATP, and water

carbon dioxide, glucose, and water

16.All of the following are correct about energy except:

The biological world gets its energy from the sun.

Chemical bonds store potential energy.

A boulder perched on a hill has kinetic energy.

Energy is defined as the ability to do work.

All forms of energy can be converted to heat.

17.What is needed for the end product of glycolysis, pyruvate,to enter the citric acid cycle?

More glucose for energy

ATP

Oxygen

Carbon dioxide

18.The enzyme that forms a transmembrane channel in mitochondriaand phosphorylates ADP

a carrier protein

ATP synthase

acetyl CoA

19.Fermentation is most common in

plants

microorganisms

animals

20.During adsorption of sunlight by photosystems, H+ ions aregenerated. Where do they come from? What are they used for?

from the breakdown of sugar; they help form water

water; they help form sugar

from carbon dioxide; they help dissolve NaCl

21.Glycolysis

does not use oxygen

uses oxygen

uses carbon dioxide

22.Photosynthesis is

not dependent on chlorophyll

a process that produces glucose and oxygen

a process that produces water and carbon dioxide

23.Breakdown of glucose generates many ATP molecules, each ofwhich can be used independently. Why is ATP ideally suited to powerbiological reactions?

ATP has many hydrogen bonds

ATP has enough energy to power one biological reaction

ATP readily dissolves in water

24.Objects that are not actively moving but have the capacity todo so are said to possess:

kinetic energy

entropy

potential energy

living energy

25.The first stage of cellular respiration, called ___________,takes place in the cytoplasm of the cell and needs no oxygen.

photorespiration

citric acid cycle

glycolysis

oxidation

26.Diffusion

requires energy

utilizes proteins to move molecules across a membrane

moves molecules against a concentration gradient

does not require energy

cannot occur without a membrane present

27.What is the name of the molecule on which an enzymeworks?

substrate

monomer

polymer

28.ATP contains

phenylalanine

two phosphate groups

three nitrate groups

three phosphate groups

29.How does chlorophyll function in photosynthesis?

by absorbing carbon dioxide

by absorbing the sun's energy

by absorbing water

30.Objects that are moving are said to possess:

living energy

potential energy

entropy

kinetic energy

31.The respiration pathway that evolved first is probably

glycolysis

aerobic respiration

citric acid cycle

32.The energy source for the process of photosynthesis is

oxygen

sunlight

carbon dioxide

chlorophyll

glucose

33.Burning wood generates heat and light. What type of reactionis this?

exergonic

kinetic energy

endergonic

potential energy

equilibrium

34.What is meant by a âcoupled reactionâ in terms of energy?

many poymers are built simultaneously

energy released by one reactions powers another reaction

some reactions occur in the same organelle

35.The First Law of Thermodynamics states:

energy is constantly being created by entropy events

energy can be changed from one form to another, but cannot becreated or destroyed

energy can be used and then destroyed because of entropy'sactions on it

energy can be destroyed while it is producing entropy

36.How do we dispose of the carbon derived from the glucose thatis metabolized during respiration?

by breathing out

via our urine

it is broken down in lysosomes

37.Both plant and animal cells have mitochondria because theyboth

carry on respiration

carry on photosynthesis.

require water

38.What is Activation Energy?

the energy needed to initiate a reaction

the energy that transports water into cells

potential energy

39.If you put a plant in a chamber and shine a light on it

oxygen will decrease and carbon dioxide will increase

oxygen will increase and carbon dioxide will decrease

oxygen and carbon dioxide will increase

oxygen and carbon dioxide will decrease

40.What are the inputs and the output molecules for the overallphotosynthetic process?

input sugar and oxygen; output carbon dioxide and water

input oxygen and water; output sugar and carbon dioxide

input carbon dioxide and water;output sugar and oxygen

41.What kind of reaction is photosynthesis?

endergonic

kinetic energy

exergonic

potential energy

equilibrium

42.In the process of glycolysis, glucose is cleaved into a pairof three-carbon molecules called

lactate

pyruvate

acetyl CoA

ATP

alcohol

43.Entropy is

order

disorder

complexity

Both order and disorder are correct

Both complexity and disorder are correct

44.Glycolysis takes place in the _____________ and the citricacid cycle and electron transport chain take place in the___________.

cytoplasm; endoplasmic reticulum

mitochondria, chloroplast

mitochondria; cytoplasm

cytoplasm; mitochondria

45.The organelle that carries out photosynthesis in plants isthe

mitochondria

chloroplast

ribosome

chlorophylllysosome

46.The energy to power the Calvin cycle comes from

cellular respiration

oxygen

the light reactions of photosynthesis

47.Which of the following can be broken down into intermediateproducts that enter cellular respiration?

Proteins

Lipids

Carbohydrates

All of these.

48.When cellular product levels get too high, the responsibleenzyme is inhibited. This is an example of

promotion

denaturation

equilibrium

a coenzyme

feedback inhibition

49.How is respiration the opposite of photosynthesis?

respiration breaks sugar down to carbon dioxide; photosynthesisbuilds sugar from carbon dioxide

respiration builds sugar from carbon dioxide; photosynthesisbreaks sugar down to carbon dioxide

respiration requires energy input; photosynthesis gives offexcess energy

50.The molecule that absorbs sunlight for photosynthesis is

oxygen

carbon dioxide

chlorophyll

glucose

sunlight

amaranthbear841

Summarize the following reading (Nutrient (zinc and vitamin E)-gene interactions related to inflammatory and antioxidant response in aging and inflammation) and it should be at least one paragraph (100-200 words) and include the following information:

* Main point of the reading

* Describe how the health deviations you read about alter normal physiology.

* Provide your key take away from the reading. This could be something that made you pause, changed your thinking, supported your thinking, or made you question something.

INTRODUCTION Aging is an inevitable biological process that is accompanied by gradual and spontaneous biochemical and physiological changes including increased susceptibility to diseases, adverse environmental conditions, and loss of mobility and agility. Alterations in neuroendocrine-immune interactions as well as in antioxidant capacity also play a fundamental role in aging. The inability of an organism to remodel these changes may lead to the appearance of some degenerative age-related diseases. As a result, the remodeling theory of aging has been proposed (1). Various nutritional factors are directly linked to these phenomena, as, for instance, in restoring the neuroendocrine-immune network, metabolic harmony, and the capacity to respond to oxidative stress (2). Approximately 40 micro nutrients (vitamins, essential minerals, and other compounds required in small amounts for normal metabolism) have been reported as essential components in the diet (3). The dietary intake of essential macro nutrients and micronutrients is usually inadequate in the elderly (4). Several causes contribute to this gap. First of all, the poor socio-economic conditions in which a large part of the older population live may lead to a consumption of inexpensive foods deficient in micronutrients, such as carbohydrates (5). The gap is worsened by the loss of appetite, lack of teeth, intestinal malabsorption, and decreased requirements for energy that lead finally to frailty, disability, and mortality (6). Some authors have reported that the deficiency of macro nutrients and micronutrients in aging is strictly related to global impairments of immune functions, metabolic harmony, and antioxidant defense by external noxae with subsequent appearance of age-related diseases (7). Indeed, many micronutrients contribute directly or indirectly to the biological activity of some antioxidant enzymes (e.g., SOD, GPx, and catalase) (8), to the efficiency of the immune system (9), and to the maintenance of metabolic function especially in preventing mitochondrial decay (4). In this last context, feeding studies in older rats have shown that mitochondrial metabolites and antioxidants protect neuronal cells from neurotoxin- and oxidant-induced toxicity and oxidative damage, delay the normal senescence of human diploid fibroblasts, and inhibit the oxidant-induced acceleration of senescence (10). With advancing age, increased oxidative damage to proteins and lipid membranes, particularly in mitochondria, causes a deformation of the structure of enzymes, with a consequent decrease in enzyme activity as well as substrate binding affinity for their substrates. An increased level of the substrate by micro nutrients restores the speed of the reaction as well as mitochondrial function, thus delaying mitochondrial decay and aging (10, 11). In contrast, recent longitudinal studies of dietary daily intake in human nonagenarians and centenarians (successful aging) have shown that an adequate consumption of micronutrients and macronutrients, as well as a satisfactory content of some trace elements within the cells, leads to good performance in several immune functions, metabolic compensation, and preservation of antioxidant activity (12, 13). In this context, polyunsaturated fatty acids, highly sensitive to reactive oxygen species, decrease in liver mitochondria from human centenarians, a feature acquired during evolution as a protective mechanism to favor longevity (14). Therefore, nutritional factors may play a pivotal role for healthy aging and longevity. However, the effects of the nutritional factors are strongly influenced by genetic factors, in particular by the genes involved in inflammatory/immune responses. Proinflammatory cytokines such as IL-1, IL-6, and TNF-Î±; the antiinflammatory cytokine IL-10; the HSP70 chaperones; and the regulators of trace element homeostasis, metallothioneins (MTs), seem particularly relevant, taking into account that the same genes are involved in the susceptibility to major geriatric disease/disorders such as diabetes, osteoporosis, osteoarthritis, dementia, cardiovascular diseases, and infections (15, 16). Indeed this reemphasizes that up to 25% of the variation in human life span is heritable (17); the rest is due to environmental and lifestyle factors, which impact the aging process, contributing as such to a large interindividual variability. Therefore, one current challenge is to understand how the interaction between genetic factors and nutrients may influence aging and longevity, in view of the high impact on gene expression, protein production, and epigenetic mechanisms implicated in regulating the life span (18). Some dietary patterns with likely different impacts on longterm disease occurrence and survival have been identified. In this context, strong evidence for a beneficial effect of higher conformity with the Mediterranean dietary pattern on causes of death, including those of cardiovascular diseases and cancer, has been reported (19). Anyway, it is also commonly accepted that the complex interactions of multiple polymorphisms play a key role in how individuals may respond to dietary interventions (20). For each nutrient, there is a window of intake between the recommended dietary allowance (RDA), which is defined as the dietary intake sufficient to meet the requirements of 97% of healthy individuals in a particular stage of life and sex group, and the tolerable upper limit (UL), which is the highest nutrient intake that can be achieved without incurring a risk of adverse health effects for most individuals in the general population (21). Although worldwide research on genetic variations that require a different RDA or UL is still in progress, several genes and alleles have been suggested to affect nutrient utilization, including genes involved in the metabolism of folate and vitamin B12 (22), vitamin E (23), lipids (24), iron (25), and zinc (26). In this last case, it is important to note that the RDA (11 mg/day for men, and 8 mg/day for women) and UL (40 mg/day for adults) for zinc are very close (Food and Nutrition Board and Institute of Medicine, 2001). Without excluding the beneficial effects of all of these nutrients for healthy aging and longevity (27), but taking into account the pivotal role played by zinc and vitamin E in fighting oxidative stress in aging and in some age-related diseases, such as atherosclerosis (23), we herein report the studies carried out on the interrelationships between zinc and some genes related to the inflammatory/immune response (such as MT and IL-6), as well as the interactions between vitamin E and the gene expressions related to inflammation. Clinical trials of zinc and vitamin E are also reported for their possible beneficial effects on longevity or in preventing the initiation and progression of cardiovascular diseases.

ZINC-MT GENE INTERACTION MTs MTs are essential to intracellular zinc homeostasis by sequestration and release of the metal when it occurs and thereby controlling available free zinc ions (28). The cysteine sulfur ligands in the cluster structure of MT can be reduced (zinc sequestration) or oxidized (zinc release), thus with concomitant changes in the relative amount of bound and free zinc (29). MTs are genetically polymorphous protein families with subfamilies, subgroups, and various isoforms. Humans possess genes for 4 subfamilies (encoded by at least 10 functional MT genes), all located on chromosome 16: the brainspecific MT3, the squamous epitheliumâspecific MT4, and the ubiquitous MT1 and MT2 (30). One of the first functions of MT1 and MT2 is to regulate zinc homeostasis and to limit oxidative damage within the cells (28). Following an injurious stimulus, such as a transient inflammation, the subsequent oxidative stress induces the release of zinc from MT via nitric oxide (NO), to promote the activity and expression of antioxidant enzymes, including MT itself, thus reducing the oxidative damage and the consequences of the injurious stimulus (31). However, the increased expression of proinflammatory cytokines occurring in aging, leads to increased expression of MTs, which in turn sequester considerable amounts of zinc, making it less available for an efficient immune response (32). If, on the one hand, the reduced zinc ion availability in old age might indicate an excessive sequestration of zinc ions by MTs, on the other, consideration of recent findings on oxidative modification of MTs leading to their loss of function suggests also a mechanism whereby these proteins can also lose their ability to buffer the intracellular free zinc concentration (33). In this case, MTs would be unable either to bind or to consequently release zinc in response to stressors. However, it is still unclear if dysfunctional MTs can be considered a typical alteration associated with specific disease/disorders, such as hyperhomocysteinemia and type 2 diabetes, or if they are a common feature of aging. Anyway, as a consequence of the altered zinc metabolism, a large number of genes that act as zinc sensors and transcriptional activators and/or repressors are also altered in aging (34). This may have a deep impact on the regulation of zincdependent transcription factors, because they not only regulate âzinc sensitiveâ genes but also control their own transcription through positive autoregulatory mechanisms (35). Taking into account that healthy centenarians display a low MT expression and satisfactory zinc ion availability despite increases in proinflammatory cytokines (IL-6, TNF-Î±) (36), it may be suggested that this feature reflects the existence of compensatory phenomena able to counteract the effects of inflammation in these exceptional individuals. Moreover, these data suggest that a preservation of zinc homeostasis is an important feature of healthy centenarians. Therefore, the role played by the zinc-gene interaction is pivotal to successful aging and, at the same time, to escape from some age-related diseases. Since, the persistence of inflammatory stimuli over time represents the biological background favoring susceptibility to age-related diseases/ disabilities, the absence of specific ârobustâ gene variants and/or the presence of specific âfrailâ gene variants might predict, on the one hand, longevity, and on the other, the predisposition to the appearance of the more common age-related diseases, such as infections and cardiovascular diseases. In this context, it has to be considered that the genes selected, because they confer a reproductive advantage early in life, may have dangerous effects in the postreproductive period. In fact, negative selection against these harmful effects fails due to the decline of natural selection with age. This fact means that one gene that is âfavorableâ in young/adult age may be âdisadvantageousâ in aging (the antagonistic pleiotropy theory of ageing (37)). Following this perspective, the beneficial effect of inflammation, via an optimal MFT-1-MT-zinc-gene interaction, in young and adult age may become detrimental in old age (32). The recent discovery of novel polymorphisms of MT2A and MT1A supports this assumption. Indeed, older subjects carrying the AA genotype for the MT2A polymorphism display low zinc ion bioavailability, chronic inflammation by high IL-6 and altered lipid assessments, with subsequent elevated risk for atherosclerosis and type 2 diabetes (38). By contrast, a polymorphism corresponding to an A/T (asparagine/ threonine) transition at the +647 nt position in the MT1A-coding region is the most often involved in female longevity (39). Such allelic variants may be very useful tools to screen older subjects at risk for zinc deficiency on a genetic basis, taking into account that the actual methodological procedures to test âzinc statusâ are often misleading and that laboratory investigations to assay zinc ion bioavailability are scarcely reproducible and poorly applicable to clinical practice (40). In this context, a novel reproducible system for testing intracellular zinc ion bioavailability has been developed using a zinc fluorescent probe (Zynpir-1) associated with MT values, with both tests representing valid methods to detect the intracellular zinc status (41).

ZINCâINTERLEUKIN-6 GENE INTERACTION Interleukin-6 (IL-6) is a pleiotropic cytokine capable of regulating proliferation, differentiation, and activity of a variety of cell types, and it plays a pivotal role in immune response. In particular, the most important function of IL-6 is most likely as a mediator of acute phase inflammatory responses. These include the balance of the proinflammatory/antiinflammatory pathways, lymphocyte activation, and hepatocellular stimulation of acute phase protein synthesis (42). Studies of the effects of aging on inflammatory response show IL-6 to be an important âcytokine for gerontologistsâ. Recent evidence has shown that abnormally increased concentrations of IL-6 are reliable markers for functional disability and predictors of disability and mortality among the elderly (43). Moreover, IL-6 dysregulation is involved in age-related inflammatory diseases, such as cancer, lymphoma, cardiovascular diseases, osteoporosis, Alzheimerâs disease, diabetes and atherosclerosis (44). The human IL-6 gene is located on chromosome band 7p21 and consists of 5 exons and 4 introns (45). Genetic studies have identified 4 polymorphisms in the Lattanzio et al 121 promoter region of the IL-6 gene (-597G/A, -572G/C, - 373A/T, -174G/C) that have a significant effect on IL-6 expression in an in vitro system (46). A variable number of tandem repeat (VNTR) polymorphisms were found in the 3â flanking region of the IL-6 gene (C allele) (47). In humans, a polymorphism in the IL-6 promoter (A/C polymorphism at position -174) altered IL-6 gene transcription rates in vitro (48) and IL-6 levels in vivo (49). In this last paper, people carrying CC or GC genotypes are defined as C+, while those carrying GG genotypes are indicated as C-. It has been suggested that IL-6 -174G/C locus variability is capable of modulating, on the one hand, individual susceptibility to common causes of morbidity and mortality among elderly, while, on the other hand, it may play a crucial role in longevity (50). Therefore, the genetic variations of this locus of IL-6 gene are fundamental in the elderly population to better understand the intrinsic causes of the longevity. The association of these genetic variations to the possible, different immune responses is an attractive focus in elucidating the molecular mechanisms involved in immunosenescence. The genetic variations of the IL-6 -174G/C locus have been extensively studied by different groups with, however, contradictory data. BonafÃ¨ et al (51) studied IL-6 promoter genetic variability at the -174C/G locus and its effect on IL-6 levels in 700 Italians aged 60 to 110 years, including 323 centenarians. Individuals who are genetically predisposed to produce high levels of IL-6 during aging â i.e., C- men (GG genotype) â at the IL-6 -174C/G locus are disadvantaged for longevity. On the other hand, the capability of C+ individuals (CC and CG genotypes) to produce low levels of IL-6 throughout their life span appears to be beneficial for longevity, at least in men. Women have, conversely, high IL-6 serum levels later in life with respect to men, independently of -174C/G locus polymorphism (51). The inhibitory tone of estrogens on IL-6 gene expression could explain the sex-based difference (52), assuming that its long-term effects last until the extreme limits of the human life span. The major production of IL-6 in C- subjects for their whole life, including centenarians, has also been confirmed by other in vivo longitudinal studies (53). A more recent study in older and nonagenarian subjects has confirmed that IL-6 production is higher in C- carriers and that these subjects are prone to contract one of the more common age-related inflammatory pathologies such as atherosclerosis (54). Interestingly, in this last study, C- older and nonagenarian subjects also display impaired innate immune response (NK cell cytotoxicity) coupled with increased MT, zinc deficiency, and low zinc ion availability, in comparison with C+ carriers (54). A functional effect of the IL-6 -174G/C locus on MT expression and zinc-regulated genes has also been confirmed recently by targeted studies with in vitro and in vivo zinc supplementation (55, 56). These findings clearly suggest that the genetic variations of the IL-6 -174G/C locus play a key role in longevity also at a functional level, and confirm the existence of a higher number of C+ centenarians than Câ ones as previously found by BonafÃ¨ et al (51). In this context, an intriguing point is the low expression of the signal-transducing component (gp130) of the IL-6 receptor in centenarians, in comparison with the elderly, despite high circulating levels of IL-6 (57), which in turn may be inactive in centenarians (36). Therefore, inflammatory status is not so detrimental in very old age, as, in contrast, occurs in normal aging. However, the discrepancies among all of the genetic studies on the variations of the IL-6 -174G/C locus in relation to longevity in the elderly means that the subject is still unclear. Ethnic, lifestyle, and cultural differences among these populations could also play a role, as well as other undefined factors. Large-scale studies at the European level in many different ethnic populations are needed to clarify this important topic. For this reason, ZINCAGE project (www.zincage.org) has been developed, and the clarification of this point has been one of is tasks. The determination of the genetic variations of the IL-6 - 174G/C locus associated with a dietary assessment or with a comprehensive evaluation of zinc status has been reported as an useful strategy to identify older subjects who can benefit from zinc supplementation without health risks (see next paragraph).

ZINC SUPPLEMENTATION IN THE ELDERLY ON THE BASIS OF GENETIC BACKGROUND One possible cause of the discrepancies existing in the literature on the effect of zinc supplementation upon immune response and antioxidant performance in the elderly (see review in (58)) may be the choice of older subjects who effectively need zinc supplementation in strict relationship with dietary habits and inflammatory status. This fact is supported by the discovery that older subjects carrying GG genotypes (i.e., C- carriers) in the IL-6 -174G/C locus display increased IL-6 production, low intracellular zinc ion availability, and impaired innate immune responses coupled with enhanced MT (56). By contrast, older subjects carrying the GC and CC genotypes (C+ carriers) in the same IL-6 -174 locus display satisfactory intracellular zinc as well as innate immune responses. But, the more intriguing finding is that males carriers of the C+ allele are more likely to reach centenarian age than C- carriers. Therefore, older C- subjects are more likely to benefit from zinc supplementation than older C+ carriers. The distribution of the IL-6 -174 genotype is very different among the various European countries, with large differences between northern and southern European countries (58). Zinc supplementation in older C- subjects restores NK cell cytotoxicity to values present in older C+ carriers and considerably improves both zinc status, assessed by the percentage increment of granulocyte Zn (56), and stress response, assessed by the percentage increment of clusterin (CLU) expression and MT protein (58). When the genetic variations for the IL-6 polymorphism are also associated with the genetic variations of MT1A in position +647, the plasma zinc deficiency and the altered immune response are more evident (58), suggesting that the genetic variations of IL-6 and MT1A would be very useful tools for the choice of older people who effectively need zinc supplementation. These results open the hypothesis that the daily requirement for zinc might be different in elderly with a different genetic background. Such a role played by genetic background on the beneficial effects of zinc supplementation is also evident in the better control of proinflammatory cytokine and chemokine production (59), as well as in reducing the expression of genes related to inflammatory status, such as IL-1 and its receptor (55). A very intriguing point is also the beneficial effect of zinc supplementation in the cognitive performance of older individuals selected on the basis of IL-6 polymorphism (60). In any case, from a microarray analysis in vitro, zinc at a dose of 50 mM down-regulates the gene expression of proinflammatory cytokines (Fig. 1), strengthening its antiinflammatory role (56, 58).

Fig. 1 - In vitro zinc treatment (50 ÂµM) down-regulates proinflammatory cytokine expression (custom array) when refereed to the value 1 (baseline control) in human peripheral blood mononuclear cells from young adult donors. The red square represents the proinflammatory cytokines (IL-6, IL-1, and TNF pathways). Data redrawn from the Zincage Project (www.zincage.org) (61).

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BIOL 1010 Lecture Notes - Lysozyme, Lysosome, Turnover Number

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