TY - JOUR
T1 - Particles internalization, oxidative stress, apoptosis and pro-inflammatory cytokines in alveolar macrophages exposed to cement dust
AU - Ogunbileje, J. O.
AU - Nawgiri, R. S.
AU - Anetor, J. I.
AU - Akinosun, O. M.
AU - Farombi, E. O.
AU - Okorodudu, A. O.
PY - 2014/5
Y1 - 2014/5
N2 - Exposure to cement dust is one of the most common occupational dust exposures worldwide, but the mechanism of toxicity has not been fully elucidated. Cement dust (N) and clinker (C) samples collected from Nigeria and another sample of cement dust (U) collected from USA were evaluated using alveolar macrophage (NR8383) cell culture to determine the contribution of different sources of cement dust in the severity of cement dust toxicity. Cement dust particles internalization and morphologic alterations using transmission electron microscopy (TEM), cytotoxicity, apoptotic cells induction, intracellular reactive oxygen species generation, glutathione reduction, TNF-α, IL-1β, and CINC-3 secretion in alveolar macrophages (NR8383) exposed to cement dust and clinker samples were determined. Particles were internalized into the cytoplasmic vacuoles, with cells exposed to U showing increased cell membrane blebbing. Also, NR8383 exposed to U show more significant ROS generation, apoptotic cells induction and decreased glutathione. Interleukin-1β and TNF-α secretion were significantly more in cells exposed to both cement dust samples compared with clinker, while CINC-3 secretion was significantly more in cells exposed to clinker (p<0.05). Endocytosis, oxidative stress induced-apoptosis and induction of pro-inflammatory cytokines may be key mechanisms of cement dust immunotoxicity in the lung and toxicity may be factory dependent.
AB - Exposure to cement dust is one of the most common occupational dust exposures worldwide, but the mechanism of toxicity has not been fully elucidated. Cement dust (N) and clinker (C) samples collected from Nigeria and another sample of cement dust (U) collected from USA were evaluated using alveolar macrophage (NR8383) cell culture to determine the contribution of different sources of cement dust in the severity of cement dust toxicity. Cement dust particles internalization and morphologic alterations using transmission electron microscopy (TEM), cytotoxicity, apoptotic cells induction, intracellular reactive oxygen species generation, glutathione reduction, TNF-α, IL-1β, and CINC-3 secretion in alveolar macrophages (NR8383) exposed to cement dust and clinker samples were determined. Particles were internalized into the cytoplasmic vacuoles, with cells exposed to U showing increased cell membrane blebbing. Also, NR8383 exposed to U show more significant ROS generation, apoptotic cells induction and decreased glutathione. Interleukin-1β and TNF-α secretion were significantly more in cells exposed to both cement dust samples compared with clinker, while CINC-3 secretion was significantly more in cells exposed to clinker (p<0.05). Endocytosis, oxidative stress induced-apoptosis and induction of pro-inflammatory cytokines may be key mechanisms of cement dust immunotoxicity in the lung and toxicity may be factory dependent.
KW - Cement dust
KW - Endocytosis
KW - Lung
KW - Oxidative stress induced-apoptosis
KW - Pro-inflammatory cytokines
UR - http://www.scopus.com/inward/record.url?scp=84899557586&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84899557586&partnerID=8YFLogxK
U2 - 10.1016/j.etap.2014.03.021
DO - 10.1016/j.etap.2014.03.021
M3 - Article
C2 - 24769344
AN - SCOPUS:84899557586
SN - 1382-6689
VL - 37
SP - 1060
EP - 1070
JO - Environmental Toxicology and Pharmacology
JF - Environmental Toxicology and Pharmacology
IS - 3
ER -