Myopathies in broiler chickens: The roles of oxidative damage and vitamin E

DA Sandercock*, MA Mitchell

*Corresponding author for this work

Research output: Contribution to journalMeeting Abstract

Abstract

Recent studies have shown that disruptions in intracellular calcium (Ca2+) homeostasis play a major role in the development of skeletal muscle damage (myopathy) in broilers. Elevations of intracellular free calcium result in Ca2+-activation of phospholipase A2 (PLA2) and the subsequent initiation of a cascade of pro-inflammatory mediators and oxygen-derived free radical generation. The ultimate consequence of free radical induced membrane lipid peroxidation is altered cell membrane integrity and thus pro-oxidative mechanisms may be central in the pathogenesis of myopathy. Vitamin E (α-tocopherol) plays an important role as a naturally occurring lipid soluble antioxidant acting as a free radical scavenger and may therefore prevent myopathy mediated by the above mechanisms. This study employed an isolated in vitro broiler chicken skeletal muscle preparation to examine the potential role of vitamin E in Ca2+-mediated oxidative membrane damage. Muscle damage was assessed by the measurement of CK in the incubation medium. Tissue calcium accumulation was estimated by 45Ca uptake. Membrane lipid peroxidation was determined by malondialdehyde (MDA) measurement. Incubation with Ca2+-ionophore significantly (p<0.001) increased muscle 45Ca2+ uptake (2.2-fold), MDA concentration (2.5-fold) and CK efflux (12-fold). Incubation with α-tocopherol (250 μM) significantly reduced MDA concentration (26%) and CK efflux (37%) but not 45Ca2+ accumulation (18%; p=0.061). In a related in vivo study, broilers from fast (FG) and slow growing (SG) lines were reared with a dietary supplementation of vitamin E (500mg/kg) and subjected to acute oxidative stress (high thermal load-31°C/75%RH, 2h). FG birds exhibited a marked myopathic response, which was significantly reduced by vitamin E supplementation (p<0.05). It is suggested that vitamin E may exert protective actions in birds during spontaneous and stress induced myopathies. Its mechanism of action may involve inhibition of lipid peroxidation and/or PLA2 activity.
Original languageEnglish
Article numberAbstract 180
Pages (from-to)43
Number of pages1
JournalPoultry Science
Volume82
Issue number1
Publication statusPrint publication - 2003
Externally publishedYes
Event92nd Poultry Science Association Annual Meeting 2003 - University of Wisconsin, Madison, United States
Duration: 6 Jul 20039 Jul 2003
https://www.poultryscience.org/abstracts.asp

Fingerprint

muscular diseases
Muscular Diseases
Vitamin E
vitamin E
Chickens
broiler chickens
calcium
Malondialdehyde
Lipid Peroxidation
Tocopherols
Phospholipases A2
Membrane Lipids
Calcium
malondialdehyde
Free Radicals
Birds
lipid peroxidation
phospholipase A2
Skeletal Muscle
tocopherols

Keywords

  • Myopathy
  • Broiler chicken
  • Oxidative damage
  • Vitamin E
  • Alpha-tocopherol
  • Myoprotective effect
  • Membrane lipid peroxidation
  • Malondialdehyde
  • Creatine kinase

Cite this

@article{df3f2f2876ec4cad8c7165466865849b,
title = "Myopathies in broiler chickens: The roles of oxidative damage and vitamin E",
abstract = "Recent studies have shown that disruptions in intracellular calcium (Ca2+) homeostasis play a major role in the development of skeletal muscle damage (myopathy) in broilers. Elevations of intracellular free calcium result in Ca2+-activation of phospholipase A2 (PLA2) and the subsequent initiation of a cascade of pro-inflammatory mediators and oxygen-derived free radical generation. The ultimate consequence of free radical induced membrane lipid peroxidation is altered cell membrane integrity and thus pro-oxidative mechanisms may be central in the pathogenesis of myopathy. Vitamin E (α-tocopherol) plays an important role as a naturally occurring lipid soluble antioxidant acting as a free radical scavenger and may therefore prevent myopathy mediated by the above mechanisms. This study employed an isolated in vitro broiler chicken skeletal muscle preparation to examine the potential role of vitamin E in Ca2+-mediated oxidative membrane damage. Muscle damage was assessed by the measurement of CK in the incubation medium. Tissue calcium accumulation was estimated by 45Ca uptake. Membrane lipid peroxidation was determined by malondialdehyde (MDA) measurement. Incubation with Ca2+-ionophore significantly (p<0.001) increased muscle 45Ca2+ uptake (2.2-fold), MDA concentration (2.5-fold) and CK efflux (12-fold). Incubation with α-tocopherol (250 μM) significantly reduced MDA concentration (26{\%}) and CK efflux (37{\%}) but not 45Ca2+ accumulation (18{\%}; p=0.061). In a related in vivo study, broilers from fast (FG) and slow growing (SG) lines were reared with a dietary supplementation of vitamin E (500mg/kg) and subjected to acute oxidative stress (high thermal load-31°C/75{\%}RH, 2h). FG birds exhibited a marked myopathic response, which was significantly reduced by vitamin E supplementation (p<0.05). It is suggested that vitamin E may exert protective actions in birds during spontaneous and stress induced myopathies. Its mechanism of action may involve inhibition of lipid peroxidation and/or PLA2 activity.",
keywords = "Myopathy, Broiler chicken, Oxidative damage, Vitamin E, Alpha-tocopherol, Myoprotective effect, Membrane lipid peroxidation, Malondialdehyde, Creatine kinase",
author = "DA Sandercock and MA Mitchell",
year = "2003",
language = "English",
volume = "82",
pages = "43",
journal = "Poultry Science",
issn = "0032-5791",
publisher = "Oxford University Press",
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}

Myopathies in broiler chickens: The roles of oxidative damage and vitamin E. / Sandercock, DA; Mitchell, MA.

In: Poultry Science, Vol. 82, No. 1, Abstract 180, 2003, p. 43.

Research output: Contribution to journalMeeting Abstract

TY - JOUR

T1 - Myopathies in broiler chickens: The roles of oxidative damage and vitamin E

AU - Sandercock, DA

AU - Mitchell, MA

PY - 2003

Y1 - 2003

N2 - Recent studies have shown that disruptions in intracellular calcium (Ca2+) homeostasis play a major role in the development of skeletal muscle damage (myopathy) in broilers. Elevations of intracellular free calcium result in Ca2+-activation of phospholipase A2 (PLA2) and the subsequent initiation of a cascade of pro-inflammatory mediators and oxygen-derived free radical generation. The ultimate consequence of free radical induced membrane lipid peroxidation is altered cell membrane integrity and thus pro-oxidative mechanisms may be central in the pathogenesis of myopathy. Vitamin E (α-tocopherol) plays an important role as a naturally occurring lipid soluble antioxidant acting as a free radical scavenger and may therefore prevent myopathy mediated by the above mechanisms. This study employed an isolated in vitro broiler chicken skeletal muscle preparation to examine the potential role of vitamin E in Ca2+-mediated oxidative membrane damage. Muscle damage was assessed by the measurement of CK in the incubation medium. Tissue calcium accumulation was estimated by 45Ca uptake. Membrane lipid peroxidation was determined by malondialdehyde (MDA) measurement. Incubation with Ca2+-ionophore significantly (p<0.001) increased muscle 45Ca2+ uptake (2.2-fold), MDA concentration (2.5-fold) and CK efflux (12-fold). Incubation with α-tocopherol (250 μM) significantly reduced MDA concentration (26%) and CK efflux (37%) but not 45Ca2+ accumulation (18%; p=0.061). In a related in vivo study, broilers from fast (FG) and slow growing (SG) lines were reared with a dietary supplementation of vitamin E (500mg/kg) and subjected to acute oxidative stress (high thermal load-31°C/75%RH, 2h). FG birds exhibited a marked myopathic response, which was significantly reduced by vitamin E supplementation (p<0.05). It is suggested that vitamin E may exert protective actions in birds during spontaneous and stress induced myopathies. Its mechanism of action may involve inhibition of lipid peroxidation and/or PLA2 activity.

AB - Recent studies have shown that disruptions in intracellular calcium (Ca2+) homeostasis play a major role in the development of skeletal muscle damage (myopathy) in broilers. Elevations of intracellular free calcium result in Ca2+-activation of phospholipase A2 (PLA2) and the subsequent initiation of a cascade of pro-inflammatory mediators and oxygen-derived free radical generation. The ultimate consequence of free radical induced membrane lipid peroxidation is altered cell membrane integrity and thus pro-oxidative mechanisms may be central in the pathogenesis of myopathy. Vitamin E (α-tocopherol) plays an important role as a naturally occurring lipid soluble antioxidant acting as a free radical scavenger and may therefore prevent myopathy mediated by the above mechanisms. This study employed an isolated in vitro broiler chicken skeletal muscle preparation to examine the potential role of vitamin E in Ca2+-mediated oxidative membrane damage. Muscle damage was assessed by the measurement of CK in the incubation medium. Tissue calcium accumulation was estimated by 45Ca uptake. Membrane lipid peroxidation was determined by malondialdehyde (MDA) measurement. Incubation with Ca2+-ionophore significantly (p<0.001) increased muscle 45Ca2+ uptake (2.2-fold), MDA concentration (2.5-fold) and CK efflux (12-fold). Incubation with α-tocopherol (250 μM) significantly reduced MDA concentration (26%) and CK efflux (37%) but not 45Ca2+ accumulation (18%; p=0.061). In a related in vivo study, broilers from fast (FG) and slow growing (SG) lines were reared with a dietary supplementation of vitamin E (500mg/kg) and subjected to acute oxidative stress (high thermal load-31°C/75%RH, 2h). FG birds exhibited a marked myopathic response, which was significantly reduced by vitamin E supplementation (p<0.05). It is suggested that vitamin E may exert protective actions in birds during spontaneous and stress induced myopathies. Its mechanism of action may involve inhibition of lipid peroxidation and/or PLA2 activity.

KW - Myopathy

KW - Broiler chicken

KW - Oxidative damage

KW - Vitamin E

KW - Alpha-tocopherol

KW - Myoprotective effect

KW - Membrane lipid peroxidation

KW - Malondialdehyde

KW - Creatine kinase

M3 - Meeting Abstract

VL - 82

SP - 43

JO - Poultry Science

JF - Poultry Science

SN - 0032-5791

IS - 1

M1 - Abstract 180

ER -