PMID- 25716970
OWN - NLM
STAT- MEDLINE
DCOM- 20151123
LR  - 20150226
IS  - 1899-1505 (Electronic)
IS  - 0867-5910 (Linking)
VI  - 66
IP  - 1
DP  - 2015 Feb
TI  - N-acetylcysteine effectively diminished meconium-induced oxidative stress in 
      adult rabbits.
PG  - 101-10
AB  - Since inflammation and oxidative stress are fundamental in the pathophysiology of 
      neonatal meconium aspiration syndrome (MAS), various anti-inflammatory drugs have 
      been used in experimental and clinical studies on MAS. This pilot study evaluated 
      therapeutic potential of N-acetylcysteine in modulation of meconium-induced 
      inflammation and oxidative lung injury. Oxygen-ventilated adult rabbits were 
      intratracheally given 4 ml/kg of meconium (25 mg/ml) or saline (Sal, n = 6). 
      Thirty minutes later, meconium-instilled animals were treated with intravenous 
      N-acetylcysteine (10 mg/kg, Mec + NAC, n=6) or were non-treated (Mec, n = 6). All 
      animals were oxygen-ventilated for additional 5 hours. Total and differential 
      blood leukocyte counts were determined at baseline, and at 1, 3 and 5 h of the 
      treatment. After sacrificing animals, left lung was saline-lavaged and total and 
      differential cell counts in the bronchoalveolar lavage fluid were determined. 
      Right lung was used for biochemical analyses and for estimation of wet-dry weight 
      ratio. In lung tissue homogenate, thiobarbituric acid-reactive substances 
      (TBARS), dityrosine, lysine-lipid peroxidation (LPO) products, and total 
      antioxidant status (TAS) were detected. In isolated lung mitochondria, TBARS, 
      dityrosine, lysine-LPO products, thiol group content, conjugated dienes, and 
      activity of cytochrome c oxidase were estimated. To evaluate systemic effects of 
      meconium instillation and NAC treatment, TBARS and TAS were determined also in 
      plasma. To evaluate participation of eosinophils in the meconium-induced 
      inflammation, eosinophil cationic protein (ECP) was detected in plasma and lung 
      homogenate. Meconium instillation increased oxidation markers and ECP in the lung 
      and decreased TAS (all P<0.05). NAC treatment reduced ECP and oxidation markers 
      (all P<0.05, except of dityrosine in homogenate and conjugated dienes in 
      mitochondria) and prevented a decrease in TAS (P<0.01) in lung homogenate 
      compared to Mec group. In plasma, NAC decreased TBARS (P<0.001) and ECP, and 
      increased TAS (both P<0.05) compared to Mec group. Concluding, N-acetylcysteine 
      diminished meconium-induced inflammation and oxidative lung injury.
FAU - Mokra, D
AU  - Mokra D
AD  - Department of Physiology, Comenius University in Bratislava, Jessenius School of 
      Medicine in Martin, Martin, Slovakia. mokra@jfmed.uniba.sk.
FAU - Drgova, A
AU  - Drgova A
FAU - Mokry, J
AU  - Mokry J
FAU - Antosova, M
AU  - Antosova M
FAU - Durdik, P
AU  - Durdik P
FAU - Calkovska, A
AU  - Calkovska A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Poland
TA  - J Physiol Pharmacol
JT  - Journal of physiology and pharmacology : an official journal of the Polish 
      Physiological Society
JID - 9114501
RN  - 0 (Antioxidants)
RN  - 0 (Biomarkers)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Thiobarbituric Acid Reactive Substances)
RN  - WYQ7N0BPYC (Acetylcysteine)
SB  - IM
MH  - Acetylcysteine/*pharmacology
MH  - Age Factors
MH  - Animals
MH  - Antioxidants/*pharmacology
MH  - Biomarkers/metabolism
MH  - Disease Models, Animal
MH  - Humans
MH  - Infant, Newborn
MH  - Inflammation Mediators/metabolism
MH  - Leukocytes/drug effects/metabolism
MH  - Lipid Peroxidation/drug effects
MH  - Lung/*drug effects/immunology/metabolism
MH  - Lung Injury/chemically induced/immunology/metabolism/*prevention & control
MH  - *Meconium
MH  - Meconium Aspiration Syndrome/chemically induced/immunology/metabolism/*prevention 
      & control
MH  - Mitochondria/drug effects/metabolism
MH  - Oxidative Stress/*drug effects
MH  - Pneumonia/chemically induced/immunology/metabolism/*prevention & control
MH  - Pulmonary Edema/metabolism/prevention & control
MH  - Rabbits
MH  - Thiobarbituric Acid Reactive Substances/metabolism
MH  - Time Factors
EDAT- 2015/02/27 06:00
MHDA- 2015/12/15 06:00
CRDT- 2015/02/27 06:00
PHST- 2014/06/29 00:00 [received]
PHST- 2015/01/23 00:00 [accepted]
PHST- 2015/02/27 06:00 [entrez]
PHST- 2015/02/27 06:00 [pubmed]
PHST- 2015/12/15 06:00 [medline]
PST - ppublish
SO  - J Physiol Pharmacol. 2015 Feb;66(1):101-10.