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Advances In Animal Production Science > Copper Metabolism in Cattle > Flashcards

Copper Metabolism in Cattle Flashcards

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1
Q

Copper introduction

A
  • first shown to be essential for growth/development/haemoglobin production in lab rats in 1920s
  • grazing ruminants with chronic wasting diseases found to respond to copper therapy (e.g Sawyback - ataxic disease of newborn lambs, neuromuscular condition unable to stand)
  • copper deficient soils affecting livestock and vegetation
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2
Q

Is copper a trace element

What is a trace element

A

Yes

required in small quantities (mg/kg DM) cattle need 15-30mg/kgDM of copper

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3
Q

What is an enzyme co-factor

A

a chemical compound required by an enzyme as a catalyst

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4
Q

cytochrome c oxidase role

can copper be used as an antioxidant

A

enzyme that requires copper for respiration in the electron transport chain as an electron acceptor
responsible to generate energy for all tissues

antioxidant - prevent tissue damage from free radicles and get rid of waste produced during respiration

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5
Q

Copper in transport of other minerals

A

Hepheastin - transport of iron from intestines, influx of iron across basolateral membrane into cells of intestinal tract

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6
Q

Peptidylglycine monoxygenase

A
  • copper dependant enzyme required for generation of appetite regulating hormones
    gastrin and CCK
    serum/tissue of
  • activity in PAM rats positively correlated with dietary intake of copper
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7
Q

Copper Metabolism - absorption

A
  • occurs in duodenum
  • enters enterocytes ACTIVE transport from lumen
  • exits by active transport into blood
  • Cu2+ to Cu by brush boarder metalloenzymes at apical surface then transported across apical membrane of enterocyte by CTR1 (high affinity copper transporter
  • Cu transported into golgi network = synthesis of metalloenzymes (e.g hepheastin) OR shuttled by atox1 to ATP7A into bloodstream
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8
Q

Where does copper go after absorption

A

to the liver(copper homeostasis main organ)

Cu bound to serum albumin with transcuprien and histidine

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9
Q

Liver role

A

storage organ
regulates copper excretion in bile
secrete copper into blood for transport to tissues

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10
Q

Copper storage and excretion

A
  • liver
  • Cu uptake into hepatocytes mediated by CTR1
  • Cu binds to cytosolic copper chaperones for intracellular transport
  • after transfer across gut = enter portal vein
  • free intracellular copper stored in vesicular copper pools
  • liver fluke infestations can limit how much Cu liver can store
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11
Q

Three pools of Cu in liver

A
  • storage (mainly in MT)
  • excretion (transpored into bile)
  • transit (enters enzymes)
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12
Q

What happens if there is excess in copper supply

A

ATP7B translocates to the cell membrane and pumps copper out of cell

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13
Q

Copper transport

A

Ceruloplasmin (CP)= main transport protein - binds 6 Cu ions
consists of 90% plasma Cu
CP produced at steady rate
however studies in mice found after gene deletion for CP still metabolise copper

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14
Q

Clinical copper deficiency in ruminants signs

  • visible
  • economic
  • pathological
A
  • change coat colour (black to white wool), swayback in lambs
  • infertility (anoestrus, lack of oestrus behaviour), Reduced growth rate poor FCR (feed conversion efficiencies)
  • uneven bone growth = osteochondrosis
  • connective tissue dysfunction (e.g. lesions in ligamentum nuchse supporting neck lead to dislocation causing head to drop and create a ‘hump’
  • heart func, immune func,
  • RBC formation (haemoglobin synthesis declines)
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15
Q

Causes of copper deficiency in ruminants

A
  • primary - lack of Cu in diet (unlikly problem in UK, tolerate low Cu)
  • Secondary - antagonists affecting Cu metabolism (e.g. molybdenum, sulphur, iron, zinc) lead to copper responsive disorders
    Suttle (1990) concluded Mo+S interactions main cause of Cu deficiency
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16
Q

Why use term copper responsive disorder rather than clinical deficiency

A

may look clinically well and give it copper supplementation and its health may improve
if clinically or sub clinically deficient, respond to copper treatment

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17
Q

What do molybdenum and sulphur combine to create

A

Thiomolybdates (MoS4)
prevents absorption of copper
can cause copper deficiency
- sulphide formed by ruminal microorg from dietary sulphate/organic sulphate compounds

molybdenum only exerts limiting effect on copper retention in presence of sulphur

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18
Q

Thiomolybdates

  • what forms them
  • types and effects
A
  • Mo and S form monothiomolybdates (TM1) - breakdown acidity of abomasum
  • become TM3
  • become TM4 (tetra-thiomolybdates) collect copper, dont allow absorption
  • further along sequence = more stable
  • more Mo and S in diet = further along sequence TM formed
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19
Q

What can happen to TMs

A
  • excreted in faeces
  • absorbed into blood and excreted through bile or stored in liver. exert systematic effect on Cu metabolism in excess
  • go into tissues - thiomolybdate removes Cu, inactivates enzymes = toxic
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20
Q

What is the haemolytic phase

A

mass release of Cu into the bloodstream, excess copper induce production of superoxide radicals which cause RBC membrane damage

mass hepatic degeneration, liver breaks down, metabolic shut down

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21
Q

Clinical signs of haemolytic phase

A
  • jaundice (excessive breakdown of rbc leading to bile accumulation)
  • dark urine
  • blood dullness
  • death
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22
Q

Why are younger animals more susceptible to copper toxicity

A

higher copper absorption in young
decreased copper absorption in adults

can still look clinically heathy with build up of copper

23
Q

How much copper fed to a cow to avoid deficiency

A

10-15 mg Cu/kg DM

24
Q

Sources of copper

A
  • pasture/food/crops depending on soil Cu, drainage, herbage species
  • normal pasture range = 4-8mg/kg DM
  • low in milk
25
Q

Copper toxicity

  • another name
  • dependent on..
  • danger level
  • what does it cause
  • enzymes
  • breed susceptibility
  • EU maximum Cu
A
  • cumulative poison (excess Cu ingested)
    ~ species dependent - pigs = highly tolerant, cattle ok, sheep = low tollerence and susceptable to copper poisoning esp on concentrated diets
  • gradual accumulation until 100mg/kg fat free DM
    poisoning occurs in areas where herbage contains 10-20mg/kg DM Cu and low molybdenum levels
    ~necrosis of liver cells, jaundice (high bilirubin levels), loss appetite, death (from hepatic coma) ~ high Cu damages liver without symptoms
  • leakage of enzymes from damaged cells into blood, sudden lelease of Cu and haemolysis as a result of stressor (parturition, infection)
    ~ scottish black face = least susceptable, Texel = most
  • EU max = 15mg/kg DM Cu
    ~ care with antiprotozoal compounds = eliminte protozoa that produce sulphide that lowers CU availability (e.g. monesin)
26
Q

Teart and molybdenum levels in teart soil compared to normal

A

= condition in cattle that causes scouring and unthriftyness

- 20-100mg/kgDM (norm = 0.5-3.0)

27
Q

Crimp wool

A
  • Cu present in enzyme for disulphide bridge formation to 2 adjacent cystine molecules
  • copper absent = protein molecules in wool dont form bridge and wool stringy
28
Q

Nutritional anaemia and falling disease

A
  • produced experimentally in young pigs by diets low in Cu
  • arise easily in animals just fed milk
  • unlikely in older animals = copper supplementation unnecessary
  • copper deficincy in cattle
  • austrailia
  • progressive degeneration of myocardium
29
Q

Cu role in

  • ceruloplasmin
  • erythrocruorin
  • superoxide dismutase
  • pigments
A
  • (protein) role with release of iron from cells into plasma. Deficient = impairs ability to absorb iron, mobilise from tissues and utilise in haemoglobin synthesis
  • (protein) occurs in erythrocytes (RBC) role in oxygen metabolism = oxygen carrying haemoprotein complexes
  • part of cells antioxident system, breaksdown harmful oxygen molecules
  • ## Turacin = pigment of feathers
30
Q

Cu deficiency symptoms

A
  • anaemia
  • poor growth
  • bone disorders
  • infertility
  • depigmentation
  • gastro-intestinal disturbances
  • scouring
  • lesions in brain stem and spinal chord = associated with muscular incoordination (lack of control), occurs especially in young lambs
31
Q

Enzoonotic ataxia

A
  • pastures with low copper content (2-4mg/kg DM)
  • prevent = feed copper salt
  • study in 1977 (smith et al) determine which stage in foetal or postnatal development produces ataxic lambs
    ~ EA detected 99 days of foetal age
    ~ no lesions if ewe received supplementary copper during pregnancy
    ~ primary events responsible for EA development take place after mid term
32
Q

Swayback
- forms

What causes variable Cu absorption efficiency

A
  • causes complete paralysis and/or staggering gait on hind limbs
  • 2 forms ~ congenital (signs apparent at birth) irriversible but prevented only by ewe enough Cu in diet
    ~ onset of clinical disease dlayed for several weeks - parenteral injection of copper complexes in small doses
  • not always caused by dietary deficiency as been known on high Cu pastures
  • efficiency of copper absorption variable
    ~ 10x variation in efficiency with Scottish blackface ewes absorbing Cu from autumn pasture (1.2%) and from leafy brassicas (13.2%)
    ~ genetics influence conc of Cu in blood/brain/liver of sheep - swayback affected by genotype
    lambs given Cu supplemented diet and fishmeal retained Blackface = 6%, Texel = 13%, Suffolk = 8-9%
33
Q

McCaughern, Mckenzie and Sinclair - starch

A
  • 2020
  • found feeding higher starch conc in diet increased hepatic Cu concentration
  • so if deficient, could be a viable option
  • increased serum ceruloplasmin activity = release iron into plasma from cells
  • main effect of starch, no effective antagonist
  • pH = lower recticular ph from maize diets compared to grass
  • once fed in morning = rapid decrease in ph (metabolise nutrients, release VFA)
  • protein yield increase with high starch conc (greater FME, greater growth of microbes, to abomasum where broken down into amino acids passed onto mamary glands)
  • DMI = suplemented diets decreased (high sulphur
34
Q

Individual farm Cu intake in 2012 - results

sinclair and atkins

A
  • 50 farms involved
    measured Cu levels where cattle exposed (mixed ration, water0
  • Only 6/50 farms fed at or below 2011 UK guideline maximum of 20mg/kgDM
  • no farms feeding below requirements
  • EU limit Cu to dairy cow was = 40mg/kgDM
  • 2016 brought down to 34mg/kgDM = 10 farms above limit
  • mean intake of Cu = 258% of NRC 2001 value (12mg/kgDM)
  • most farms have tendency to oversuplement CU
35
Q

Kendall et al 2015 - liver Cu conc in cull cattle in Uk

and why dont get toxicity

A
  • separated into animal classification = beef cows, dairy Holstein, other dairy breeds
  • measured liver Cu conc above AHVLA reference range = 508mg/kgDM (%)
  • 38% Holstein dairy cull cows had higher toxic liver Cu conc which were higher than reference range
  • beef cows (lower proportion of concentrates, housed short periods, exposed to higher sulphur/molybdenum) 17% higher toxic liver Cu higher than reference range
  • Holstein breed has high tolerance for Cu toxicity (just seem dull, lethargic) rarely copper toxic clinically
36
Q

Why care about copper toxicity (health complication)

A
  • increased risk of cancer (urinary tract)

- enter food chain and impact human health

37
Q

Reasons for over supplementation of Cu

A
  • decreased fertility with suboptimal Cu supplementation = safe than sorry to prevent reduced fertility
  • copper come from variety of sources (miscommunication form nutritionist, mineral sales person sell boluses
  • high conc of sulphur/molybdenum in forage in some farms
38
Q

Effect of forage type and antagonists on hepatic Cu retention
- forage vs maize

A
  • forage with naturally high sulphur and molybdenum, nutritionists analyse
  • increase copper conc in diet
  • avoid deficiency and no toxicity due to high S/Mo conc
  • if grow maze for lactating dairy cows (high S/Mo) increase Cu to compensate
  • cows with maize drop dead of Cu toxicity = lethargic, reduced intakes/fertility/yeilds, outbreaks of Tb
39
Q

Effect of forage type and antagonists on hepatic Cu retention
(study)

A
  • Sinclair et al 2017
  • 56 cows
  • see differences between maize diet vs grass based
  • 75% maize/25% grass and then 25% maize/75% grass
  • 4 treatments = maize with/wo antagonists, grass with/wo antagonists
  • antagonists = extra S/Mo to simulate farms with naturally high cons
  • feed diets for 14 weeks each
  • monitor changes in hepatic copper conc and performance over time
  • liver sample at start of diet, at 14 weeks (calculate change per day)
  • with normal maize/grass diets both hepatic conc increased by 0.7 and 0.9 respectively
  • expect conc to go down same extent in antagonist diets due to S/Mo
  • grass based diet = di happen
  • maize = still increased in copper by 0.2mg/kgDM = S/Mo not really affect in maize
40
Q

How dairy cow diets changed and why

A
  • now in uk, increased milk yields for dairy cows
  • fed higher energy diets = substituted grass for maize
  • ## maize has more energy to drive higher milk yields
41
Q

What’s wrong with equations for calculating Cu needed for diets

A
  • initially based on smi purified grassbased diets in sheep

- dont apply to maize diets

42
Q

Why differences in Cu metabolism between dairy vs beef cattle

A
  • not taking account of maze inclusion in lactating dairy cow diets = should give lower quantities of copper
  • feed greater quantities of copper easier
  • lots of sources of copper
43
Q

Copper statistics

  • uk dairy herds feeding above industry limit 20mg/kgDM Cu
  • uk female dairy herd had toxic/high liver Cu conc
A
  • 64%

- 40%

44
Q

Affect of diets on rumen ph and dietary starch

A
  • maize silage diets = reduce pH to greater extent compared to grass based diet
  • rumen pH may have effect on type of TM formed
  • feeding maize alters dietary starch concentrations
  • dietary starch related to rapidly fermentable carbohydrates, rapid fermentation results in volatile fatty acids (esp propionic acid
  • generation of propionic acid decreases pH of rumen = affect TM formation = affect copper absorption
45
Q

Sulphur metabolism in rumen and affect on DMI

why is there a change in intake for high starch diets

A
  • inorganic or organic (containing amino acids)
  • acted on by sulphur reducing bacteria = release hydrogen sulphide (HS)
  • HS 2 pathways in rumen ~ dissociate to form bisulfide or remain as hydrogen sulphide where migrate to gas cap of rumen is eructated and inhaled, absorbed into blood streem and cauases brain damage (polioencephalomalacia)
  • sulphur acts of smooth muscle lining the rumen and slows down contraction, feedstuff retention time increases, cant eat as much full for longer, decrease intake
  • lower ruminal ph = greater proportion of hydrogen sulphide migrate to gas cap (high starch diets)
46
Q

Where does the interaction of S and Mo occur

A

ruminal fluid

47
Q

What happens when sulphur is lost from the system (rumen)

A

less sulphur around to complex copper in TM and prevent absorption

48
Q

Low starch vs high starch - hydrogen sulphide pathways

A

low = hydrogen sulphide turns to bisulfide S combine with Mo to form Thiomolybdates which results in HIGHER pH

high = hydrogen sulphide enter lungs and LOWER pH

49
Q

Measuring copper status

A
  • diet
  • liver biopsey ~ local anesthetic, 11th intercostal space, probe inserted, very invasive
  • blood ~ identifies Cu deficiency, liver enzymes enter blood when hepatocytes rupture
  • ICP-MS = measures dietary minerals (Cu, S, Mo) other factors can influence such as diet
50
Q

Why is it difficult to diagnose Cu status, toxicity and deficiency

What does diagnosis rely on

A
  • clinical signs of copper deprivation cant be relied on for diagnosis (e.g. various nutritional stresses cause loss of crimped wool in sheep
  • presence of clinical symptoms OR sub clinical loss production
  • biochemical evidence of subnormal tissue or blood copper
  • improvement after treatment with copper compares to untreated cattle
  • find def/toxicity
  • try to correct it and alter supplementation strategies
  • track performance
51
Q

How to measure Cu status from blood samples

A
  • plasma copper = icp-ms
  • ceruloplasmin = ELIZA
  • liver function enzymes e.g. AST, ALT = ELIZA
  • measure Mo levels in plasma (More Mo absorbed via intestinal wall = indicate more Cu absorbed and Mo not complex with copper ~ not in blood, removed in faeces
52
Q

How to measure Cu status in liver samples

A
  • liver Cu conc = ICP-MS
  • Adv = most accurate
  • DIs = invasive, expensive, time consuming
  • big range in deficiency and toxicity = changes with fertility and immunology even within middle range (20mg/kgDM - 508mg/kgDM
53
Q

Ways to prevent Cu deficiency

A
  • Cu containing pasture fertilisers
  • inorganic dietary supplement sources
    ~ salt licks containing 0.5-1.9% CU
    ~ Cu solution in water (small doses can cause rapid clinical response due to some Cu bypassing rumen) or forage to maintain a Cu:Mo ratio of >3
  • Organic dietary sources
    ~ Calves given 10mg/kg DM Cu as glycinate complex in corn-based diets containing 2 and later 6mg/kg DM Mo = up to 44% greater responses in plasma and liver Cu

Advances In Animal Production Science (13 decks)

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