Impairment of alveolar type-II cells involved in the toxicity of Aflatoxin G(1) in rat lung.
Our previous studies showed intragastric administration of Aflatoxin G(1) (AFG(1)) could induce lung adenocarcinoma, which derived from alveolar type II cells (AT-II cells). AT-II cells contribute to Aflatoxin B(1) (AFB(1)) metabolism and also serve as the potential progenitor cells for AFB(1)-induced tumorigenesis. Thus, AT-II cells may constitute a target for AFG(1) exposure and serve as progenitor cells for tumorigenesis induced by AFG(1). The current experiment was designed to identify the acute toxicity of AFG(1) in AT-II cells following a single intratracheal administration of AFG(1). We observed inflammatory changes in the alveolar septum at days 3 and 7 after AFG(1) treatment, which resolved by 14days. We also found AFG(1) caused lamellar bodies damage in AT-II cells at days 3 and 7 post-treatment. Surfactant protein C (SP-C) expression, an AT-II cell-specific marker, was reduced at day 7 post-treatment. The structural and functional impairment in AT-II cells returned to normal by day 14. Moreover, we found that AFG(1) induced a elevation of intracellular calcium concentration [Ca(2+)]i in AT-II cells in vitro, which may contribute to the decreased SP-C expression. In conclusion, our results show AFG(1) induces structural and functional impairment in AT-II cells involved in the acute toxicity of AFG(1) in lung.
Lab of Pathology, Hebei Medical University, Shijiazhuang, China.
Haitao
H
Shen
Ping
P
Lv
Xin
X
Xing
Lingxiao
L
Xing
Xia
X
Yan
Junling
J
Wang
Xianghong
X
Zhang
D000348:Aflatoxins / Q000633:toxicity*; D000818:Animals; D008168:Lung / Q000166:cytology / Q000187:drug effects*; D008297:Male; D011650:Pulmonary Alveoli / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction
D000348:Aflatoxins; C027955:aflatoxin G1