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Background: Paraquat
is an herbicide produced and used prevalently worldwide. Studies have shown
that lung fibrosis induced by paraquat can be prevented or delayed by certain
antioxidants, iron chelating agents, melatonin, and, recently, blood pressure
lowering drugs such as captopril.
Methods: The protective effects of captopril on paraquat
toxicity were studied using RT-PCR and immunohistochemistry to determine the gene and
protein expression of p53 and Bcl-2 in lung tissue samples from rats treated with captopril
before and after exposure to paraquat.
Results: We found no significant difference in the gene and
protein expression of p53 in different tissue samples, except for mRNA levels in the
lung tissue of captopril-treated rats. However, the protein expression of Bcl-2 is greater in tissue
from rats exposed to paraquat alone and paraquat together with pre- and
posttreatment with captopril compared to tissue from untreated control rats and
from those treated with captopril alone, which can be due to inflammatory
responses of lung tissue. By RT-PCR, we were unable to detect Bcl-2 in lung tissue
samples.
Conclusion: These results show that paraquat does not induce
significant DNA
damage therefore, the gene and protein expression of p53 was not changed.
Paraquat does induce lung tissue inflammation, which in turn increases Bcl-2 protein expression.
Finally, captopril had no significant effect on the lung tissue toxicity
induced by paraquat. Considering these results and the cellular interactions in
lung tissue, we suggest that complementary assays and in-vitro cell culture experiments be performed to further elucidate
the molecular events underlying paraquat lung toxicity.
