Protective effects of melatonin and quercetin on experimental lung injury induced by carbon tetrachloride in rats.
BACKGROUND
Exposure to carbon tetrachloride (CCl4), a well-known toxicant, causes tissue damage by inducing oxidative stress via formation of free radicals. The fundamental structure of the organs of rats and humans is similar, so administration of CCl4 to rats is an accepted experimental model to produce oxidative damage to various tissues including pulmonary tissue. In this study, we evaluated the protective capacity of melatonin and quercetin against CCl4-induced oxidative lung damage in rats.


METHODS
Rats were divided into five groups each containing seven rats as follows: Control group, Olive oil group CCl4 group, CCl4+Melatonin, and CCl4+Quercetin group. The tissue samples were processed by routine histological and biochemical procedures. Sections were stained with Hematoxylin-eosin and Masson's trichrome. Histopathologic damage score was calculated. Malondialdehyde (MDA) and glutathione (GSH) levels and catalase (CAT) activities were assayed.


RESULTS
The lung sections of control groups showed normal histological characteristics. Fibrosis, interstitial hemorrhage, epithelial desquamation in bronchiole and alveoli, intra-alveolar edema, leukocyte, and macrophage infiltration were observed in lung sections of rats exposed to CCl4 alone. The findings were reduced in the treatments groups. The MDA level in the CCI4 group were significantly higher than in the other groups (p < .001), and the CAT and GSH levels in the CCI4+Mel and CCI4+Quer groups were significantly higher than in the CCI4 group (p < .05).


CONCLUSIONS
In conclusion, we suggest that agents with antioxidant properties such as melatonin and quercetin may have positive effects in the treatment of pulmonary diseases characterized by especially edema, inflammation, and fibrosis.
1Department of Histology and Embriyology, Medical Faculty, Inonu University, Malatya, Turkey.
Elif
E
Taslidere
Mukaddes
M
Esrefoglu
Hulya
H
Elbe
Asli
A
Cetin
Burhan
B
Ates
D055371:Acute Lung Injury / Q000139:chemically induced* / Q000473:pathology / Q000517:prevention & control*; D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D002251:Carbon Tetrachloride / Q000009:adverse effects* / Q000494:pharmacology; D002374:Catalase / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D005978:Glutathione / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008315:Malondialdehyde / Q000378:metabolism; D008550:Melatonin / Q000627:therapeutic use*; D011014:Pneumonia / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control; D011654:Pulmonary Edema / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control; D011658:Pulmonary Fibrosis / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control; D011794:Quercetin / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar
D000975:Antioxidants; D008315:Malondialdehyde; D011794:Quercetin; D002251:Carbon Tetrachloride; D002374:Catalase; D005978:Glutathione; D008550:Melatonin