Publication: Pulmonary response to methylcyclopentadienyl manganese tricarbonyl treatment in rats: injury and repair evaluation
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Date
2006
Authors
Halatek, T. ; Opalska, B. ; Rydzynski, K. ; Bernard, A.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Methylcyclopentadienyl manganese
tricarbonyl (MMT), an organometallic compound, used
as an antiknock additive in fuels, may produce alveolar
inflammation and bronchiolar cell injury.
The aim of the experimental study on female rats
was to determine by morphological examination and
sensitive biomarkers, the course of the injury and repair
process following a single i.p. injection of 5 mg/kg
MMT. The animals were sacrificed 12, 24, 48 hours or 7
days post-exposure (PE). The first biochemical changes
12 h PE showed an increase in GSH-S-transferase (GST)
activity in the lung parallel to the earliest observed
morphological changes -vacuolation and swollen
cytoplasm in type I pneumocytes. Alterations in type I
pneumocytes were most prevalent in rat lung 24 h PE.
Clara cells with dilated smooth endoplasmic reticulum
membranes and cytoplasmic vacuolation could be
observed. Compared to the values found for controls,
Clara cell protein (CC16) in the bronchoalveolar lavage
fluid (BALF) at 24 and 48 h PE decreased by 58% and
55%, respectively. At the same time (at 24 and 48 h), the
total protein concentration in BALF increased 5 and 7
times, respectively. A significant rise in hyaluronic acid
(HA) level was observed 24 and 48 h PE. Divided type
II pneumocyte cells and Clara cells in their mitotic phase
were observed in immunocytochemistry (detecting BrdU
binding into DNA) 48 h PE. Seven days after MMT
administration, fibroblasts, macrophages, collagen and
elastin fibres could be seen in the alveolar walls as well
as neutrophils, lymphocytes, and alveoli macrophages in
the alveolar lumen. We conclude that injury and repair of
bronchial epithelium cells, especially of Clara cells and
type II pneumocyte cells, play an important part in MMT toxicity, probably depending on the antioxidant status of
these cells. The sensitive biomarkers of CC16 and
hyaluronic acid in BALF and serum reflect lung injury
and indicate the time course of pulmonary damage and
repair processes.
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