Influence of alpha-lipoic acid on nicotine-induced lung and liver damage in experimental rats.
Nicotine mediates some of the injurious effects caused by consuming tobacco products. This work aimed at investigating the defensive role of alpha-lipoic acid (ALA) with its known antioxidant and antiinflammatory effect in nicotine-induced lung and liver damage. Rats were arranged into 4 groups: control, nicotine, ALA, and ALA-nicotine groups. Oxidative stress and antioxidant status were determined by assessing thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), and glutathione (GSH) levels in lung and liver. Liver enzymes and lipid profiles were measured and pulmonary and hepatic damage were assessed by histopathological examination. Also, serum levels of transforming growth factor beta 1 (TGF-β1) and vascular cell adhesion molecule 1 (VCAM-1) were determined. The results revealed an increase in TBARS in tissues and a reduction in both SOD and GSH activity in the nicotine-treated rats. Nicotine induced high levels of liver enzymes, TGF-β1, VCAM-1, and dyslipidemia with histopathological changes in the lung and liver. ALA administration along with nicotine attenuated oxidative stress and normalized the SOD and GSH levels, ameliorated dyslipidemia, and improved TGF-β1 and VCAM-1 with better histopathology of the lung and liver. The study data revealed that ALA may be beneficial in alleviating nicotine-induced oxidative stress, dyslipidemia, and both lung and liver damage.
a College of Pharmacy, Taibah University, Al-Madinah Al-Munawarah, Saudi Arabia.|b Department of Clinical Pharmacology, Faculty of Medicine, Cairo University, Egypt.
Hayam
H
Ateyya
a College of Pharmacy, Taibah University, Al-Madinah Al-Munawarah, Saudi Arabia.|c Faculty of Pharmacy, Mansoura University, Egypt.
Manar A
MA
Nader
d Department of Anatomy, Faculty of Medicine, Taibah University, Al-Madinah Al-Munawarah, Saudi Arabia.|e Department of Histology and Cell Biology, Faculty of Medicine, Mansoura University, Al Mansoura, Egypt.
Ghalia M
GM
Attia
f Department of Pharmacology and Toxicology, College of Pharmacy, Taibah University, Al-Madinah Al-Munawarah, Saudi Arabia.|g Department of Clinical Pharmacology, Faculty of Medicine, Suez Canal University, Egypt.
Nagla A
NA
El-Sherbeeny
D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D050171:Dyslipidemias / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D008168:Lung / Q000187:drug effects* / Q000378:metabolism* / Q000473:pathology; D008297:Male; D009538:Nicotine / Q000009:adverse effects*; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D008063:Thioctic Acid / Q000494:pharmacology*; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
D000975:Antioxidants; D053773:Transforming Growth Factor beta1; D019010:Vascular Cell Adhesion Molecule-1; D009538:Nicotine; D008063:Thioctic Acid
acide alpha lipoïque; alpha-lipoic acid; dyslipidemia; dyslipidémie; molécule d’adhésion cellulaire vasculaire 1; nicotine; oxidative stress; stress oxydatif; vascular adhesion molecule-1