Immune Alterations, Lipid Peroxidation, and Muscle Damage Following a Hill Race

2005 ◽  
Vol 30 (2) ◽  
pp. 196-211 ◽  
Author(s):  
Richard J. Simpson ◽  
Martin R. Wilson ◽  
James R. Black ◽  
James A. Ross ◽  
Greg P. Whyte ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Muscle Damage ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Acute Phase Proteins ◽  
Venous Blood ◽  
Total Antioxidant Status ◽  
Phase Response ◽  
Tnf Α

Hill races usually include large downhill running sections, which can induce significant degrees of muscle damage in a field setting. This study examined the link between muscle damage, oxidative stress, and immune perturbations following a 7-km mountainous hill race with 457 m of ascent and 457 m of descent. Venous blood samples were taken from 7 club level runners before, immediately after, and 48 hrs postrace. Samples were analysed for total and differential leukocyte counts, markers of muscle damage (CK), lipid peroxidation (MDA), and acute phase proteins (CRP; fibrinogen; α-1-ACT). The total antioxidant status (TEAC) and plasma levels of the proinflammatory cytokines IL-6, IL-8, and TNF-α were also determined. Subjective pain reports, and plasma activities of CK, MDA, and circulatory monocytes reached peak values at 48 hrs postrace (p <  0.05). TEAC and the cytokine IL-8 increased immediately after the race (p <  0.05). Plasma TNF-α remained unchanged (p > 0.05). Despite the reports of muscle damage and soreness, no evidence of an acute phase response was observed (p > 0.05), which may be explained by the failure of the race to induce a plasma TNF-α response. Future studies should examine the link between muscle damage, oxidative stress, and the acute phase response following hill races of longer duration with larger eccentric components. Key words: acute phase response, cytokines, antioxidant capacity, creatine kinase, field study

Effects of eprinomectin administration on apoptosis, acute phase response and antioxidant status in cattle

2019 ◽  
Author(s):  
H. Aksit ◽  
D. Aksit
Keyword(s):  
Acute Phase ◽  
Total Protein ◽  
Acute Phase Response ◽  
Antioxidant Status ◽  
Acute Phase Proteins ◽  
Total Antioxidant Status ◽  
Phase Response ◽  
Total Antioxidant ◽  
Liver And Kidney ◽  
Group 2

Eprinomectin is a broad spectrum endectocides used against gastrointestinal, pulmonary nematodes and ectoparasites in cattle. The main objective of the present study was to investigate effects of eprinomectin in cows following subcutaneous and pour-on administrations; on serum DNA apoptosis, acute phase response, Total Antioxidant Status (TAS), total protein, creatinine, urea levels, and AST, ALT and GGT activities. Ten Holstein cows were divided into two groups. Group 1 received subcutaneous (0.2 mg/kg) and group 2 received pour-on (0.5 mg/kg) administration of eprinomectin. Blood samples were collected from vena jugularis prior to and following the drug administration at intervals of 36 hrs, 3rd, 6th, 12nd and 20th days, respectively. Samples were centrifuged at 2500 g for 15 minutes and separated sera stored at -20 ºC. Results showed that the eprinomectin application decreases the sera levels of acute phase proteins. Statistically significant increase was observed in antioxidant capasity (P less than 0.05) and total protein (P less than 0.01). However, there was non-significant increase in apoptosis rate. No remarkable alterations were observed in AST, ALT and GGT activities including urea and creatinine levels. Results showed that the eprinomectin application reduces the sera levels of acute phase proteins (ceruloplasmin and sialic acid) in cows. However, statistically significant increase was measured in antioxidant capasity (P less than 0.05) and total protein (P less than 0.01) levels. It could be concluded from the study that eprinomectin do not have adverse effects on liver and kidney.

Regulation of urea synthesis during the acute-phase response in rats

2013 ◽  
Vol 304 (7) ◽  
pp. G680-G686 ◽  
Author(s):  
Karen Louise Thomsen ◽  
Niels Jessen ◽  
Andreas Buch Møller ◽  
Niels Kristian Aagaard ◽  
Henning Grønbæk ◽  
...  
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Urea Cycle ◽  
Acute Phase Proteins ◽  
Phase Response ◽  
Mrna Levels ◽  
Urea Synthesis ◽  
Cycle Enzyme ◽  
Tnf Α ◽  
Urea Cycle Enzyme

The acute-phase response is a catabolic event involving increased waste of amino-nitrogen (N) via hepatic urea synthesis, despite an increased need for amino-N incorporation into acute-phase proteins. This study aimed to clarify the regulation of N elimination via urea during different phases of the tumor necrosis factor-α (TNF-α)-induced acute-phase response in rats. We used four methods to study the regulation of urea synthesis: We examined urea cycle enzyme mRNA levels in liver tissue, the hepatocyte urea cycle enzyme proteins, the in vivo capacity of urea-N synthesis (CUNS), and known humoral regulators of CUNS at 1, 3, 24, and 72 h after TNF-α injection (25 μg/kg iv rrTNF-α) in rats. Serum acute-phase proteins and their liver mRNA levels were also measured. The urea cycle enzyme mRNA levels acutely decreased and then gradually normalized, whereas the urea cycle enzyme proteins remained essentially unchanged over time. The CUNS rose after 3 h and then normalized. The acute-phase response was fully activated at 24 h with markedly increased serum levels of the acute-phase proteins. TNF-α acutely upregulated the CUNS. Later, despite the fully established 24-h acute-phase response and the decreased activity of the urea cycle enzyme genes, there was no change in the urea cycle enzyme proteins or the CUNS. Thus in no phase after the initiation of the acute-phase response was in vivo urea synthesis orchestrated in combination with acute-phase protein synthesis so as to limit N waste.

scholarly journals Effects of mild zinc deficiency, plus or minus an acute-phase response, on galactosamine-induced hepatitis in rats

1994 ◽  
Vol 72 (4) ◽  
pp. 611-618 ◽  
Author(s):  
Susan E. Parsons ◽  
Robert A. Disilvestro
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Acute Phase Proteins ◽  
Phase Response ◽  
Zn Deficiency ◽  
Protective Mechanisms ◽  
Antioxidant Function ◽  
Zn Status

Zn deficiency is hypothesized to produce poor resistance to injury involving oxidative stress. This could occur by impairing Zn antioxidant function(s) or by indirectly limiting adaptive protective mechanisms such as a rise in acute-phase proteins. The present study examined rats fed diets adequate or moderately low in Zn (4 or 25 μg/g diet) for 9 d. The lower intake produced a mild Zn deficiency based on body weight, plasma Zn and plasma alkaline phosphatase (EC 3.1.3.1) activity. Galactosamine injection, an oxidative stress, produced much more liver injury in the mildly Zn-deficient rats. However, injury was strongly inhibited in rats from each dietary group by an acute-phase response due to turpentine-induced leg inflammation. Mild Zn deficiency did not prevent a rise in levels of the acute-phase protein caeruloplasmin (EC 1.16.3.1), but did limit the usual inflammation-induced rise in hepatic levels of metallothionein, a Zn protein with possible antioxidant function. In conclusion, high degrees of galactosamine-induced hepatitis were associated with mild Zn deficiency, but the liver injury was blocked by prior stimulation of an acute-phase response, regardless of Zn status.

The acute phase response and C-reactive protein

2020 ◽  
pp. 2199-2207
Author(s):  
Mark B. Pepys
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Serum Amyloid A ◽  
Acute Phase Proteins ◽  
Phase Response ◽  
Serum Amyloid ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Amyloid A ◽  
Serum Amyloid A Protein

The acute phase response—trauma, tissue necrosis, infection, inflammation, and malignant neoplasia induce a complex series of nonspecific systemic, physiological, and metabolic responses including fever, leucocytosis, catabolism of muscle proteins, greatly increased de novo synthesis and secretion of a number of ‘acute phase’ plasma proteins, and decreased synthesis of albumin, transthyretin, and high- and low-density lipoproteins. The altered plasma protein concentration profile is called the acute phase response. Acute phase proteins—these are mostly synthesized by hepatocytes, in which transcription is controlled by cytokines including interleukin 1, interleukin 6, and tumour necrosis factor. The circulating concentrations of complement proteins and clotting factors increase by up to 50 to 100%; some of the proteinase inhibitors and α‎1-acid glycoprotein can increase three- to fivefold; but C-reactive protein (CRP) and serum amyloid A protein (an apolipoprotein of high-density lipoprotein particles) are unique in that their concentrations can change by more than 1000-fold. C-reactive protein—this consists of five identical, nonglycosylated, noncovalently associated polypeptide subunits. It binds to autologous and extrinsic materials which contain phosphocholine, including bacteria and their products. Ligand-bound CRP activates the classical complement pathway and triggers the inflammatory and opsonizing activities of the complement system, thereby contributing to innate host resistance to pneumococci and probably to recognition and safe ‘scavenging’ of cellular debris. Clinical features—(1) determination of CRP in serum or plasma is the most useful marker of the acute phase response in most inflammatory and tissue damaging conditions. (2) Acute phase proteins may be harmful in some circumstances. Sustained increased production of serum amyloid A protein can lead to the deposition of AA-type, reactive systemic amyloid.

scholarly journals Alteration of Transthyretin Microheterogeneity in Serum of Multiple Trauma Patients

2007 ◽  
Vol 2 ◽  
pp. 117727190700200 ◽  
Author(s):  
Beate Gericke ◽  
Jens Raila ◽  
Maria Deja ◽  
Sascha Rohn ◽  
Bernd Donaubauer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Multiple Trauma ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Injury Severity ◽  
Phase Response ◽  
Linear Matrix ◽  
Trauma Patients ◽  
Flight Mass Spectrometry ◽  
Multiple Trauma Patients

Transthyretin (TTR) which exists in various isoforms, is a valid marker for acute phase response and subclinical malnutrition. The aim of the study was to investigate the relationship between inflammation, oxidative stress and the occurrence of changes in microheterogeneity of TTR. A prospective, observational study at a level-I trauma center of a large urban medical university was performed. Patients were severely injured (n = 18; injury severity score (ISS): 34–66), and were observed within the first 24 hours of admittance and over the following days until day 20 after injury. 20 healthy subjects, matched by age and sex, were used as controls. TTR was enriched by immunoprecipitation. Microheterogeneity of TTR was determined by linear matrix assisted laser desorption/ionization-time of flight-mass spectrometry (MALDI-TOF-MS). Four major mass signals were observed for TTR representing native, S-cysteinylated, S-cysteinglycinylated and S-glutathionylated TTR. In the course of their ICU stay, 14 of the 18 patients showed a transient change in microheterogeneity in favour of the S-cysteinglycinylated form of TTR (p < 0.05 vs. controls). The occurrence of this variant was not associated with the severity of trauma or the intensity of the acute-phase response, but was associated with oxidative stress as evidenced by Trolox. Our results demonstrate that changes in microheterogeneity of TTR occur in a substantial number of ICU trauma patients. The diagnostic values of these changes remains to be elucidated. It is speculated that TTR modification may well be the mechanism underlying the morphological manifestation of amyloidose or Alzheimer's diseases in patients surviving multiple trauma.

Relation Among Neutrophil Enzyme Activity, Lipid Peroxidation, and Acute-Phase Response in Foal Heat in Mares

2014 ◽  
Vol 34 (11-12) ◽  
pp. 1286-1293 ◽  
Author(s):  
Joanna Wessely-Szponder ◽  
Leszek Krakowski ◽  
Ryszard Bobowiec ◽  
Elżbieta Tusińska
Keyword(s):  
Lipid Peroxidation ◽  
Enzyme Activity ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Phase Response

Follistatin concentrations in male sheep increase following sham castration/castration or injection of interleukin-1β

1996 ◽  
Vol 151 (1) ◽  
pp. 119-124 ◽  
Author(s):  
D J Phillips ◽  
M P Hedger ◽  
J R McFarlane ◽  
R Klein ◽  
I J Clarke ◽  
...  
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Interleukin 2 ◽  
Inhibitory Effect ◽  
Phase Response ◽  
Interleukin 1Β ◽  
Tnf Α ◽  
Recombinant Interleukin 2 ◽  
Factor Α ◽  
Male Sheep

Abstract Plasma follistatin (FS) concentrations were determined after castration (n=5) or sham castration (n=4) of mature rams. Both treatments resulted in a prolonged increase in FS between 7 and 19 h after surgery, which returned to pretreatment concentrations by 24 h. Tumour necrosis factor-α (TNF-α), a sensitive marker of an acute-phase response, was undetectable in plasma, indicating that the FS response was not induced by trauma due to surgery. In a second experiment, injection of castrated rams (n=4) with ovine recombinant interleukin-1β, an acute-phase mediator, resulted in a sustained rise in FS concentrations within 4 h of injection. Plasma TNF-α concentrations increased transiently within 1 h of interleukin-1β injection, indicating that an acute-phase response had been initiated. Plasma follicle-stimulating hormone (FSH) concentrations were significantly decreased at 8 and 24 h after interleukin-1β injection, strongly suggestive of an inhibitory effect of increased FS concentrations on the secretion of FSH. Injection of castrated rams (n=2) with a control preparation of recombinant interleukin-2 did not induce an acute-phase response, and plasma FS and FSH concentrations were unaffected. These data show that the testis is not a major source of circulating FS, that the increase in circulating FS following sham castration/castration is not due to an acute-phase response, but that conversely FS concentrations are modulated by the acute-phase mediator, interleukin-1β. Journal of Endocrinology (1996) 151, 119–124

scholarly journals Monokines regulate glycosylation of acute-phase proteins.

1987 ◽  
Vol 166 (1) ◽  
pp. 253-258 ◽  
Author(s):  
A Mackiewicz ◽  
M K Ganapathi ◽  
D Schultz ◽  
I Kushner
Keyword(s):  
Cell Line ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Acute Phase Proteins ◽  
Hepatoma Cell ◽  
Phase Response ◽  
Hepatoma Cell Line ◽  
Human Hepatoma Cell ◽  
Inflammatory Stimuli ◽  
Necrosis Factor

The acute-phase response to inflammatory stimuli, characterized by increased synthesis of acute-phase proteins (APP), is often accompanied by changes in the glycosylation patterns of some of these proteins. While expression of APP genes in hepatocytes is regulated by monokines, mechanisms governing changes in glycosylation are not known. Exposure of human hepatoma cell line Hep 3B to conditioned medium from LPS-activated human monocytes and to medium from the keratocarcinoma cell line COLO-16 led to increased synthesis of alpha 1 proteinase-inhibitor and ceruloplasmin and to alterations of their glycosylation patterns similar to those seen in human serum in various inflammatory states. IL-1, tumor necrosis factor, and hepatocyte stimulating factor I increased synthesis of ceruloplasmin without alterations in the pattern of its glycosylation. These findings demonstrate that altered glycosylation seen in plasma in some inflammatory states can be explained by the effects of monokines on glycosylation in hepatocytes and that gene expression and glycosylation of some APP during the acute-phase response may be regulated by different mechanisms.

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