The protective effect of melatonin on nicotine-induced myocardial injury in newborn rats whose mothers received nicotine.
OBJECTIVE
Nicotine, one of the most dangerous substances in tobacco, can pass the placenta and affect the fetal hemodynamics. The aim of this study was to evaluate the protective effects of melatonin on hearts of nicotine exposed newborn rats whose mothers received nicotine.


METHODS
This is an experimental, randomized, controlled study. Study groups were composed of five groups of rats; high-dose nicotine (HDN), HDN+melatonin (HDNM), low-dose nicotine (LDN), LDN+melatonin (LDNM), control. Myocardial and plasma malondialdehyde (MDA), nitric oxide(NO), glutathione peroxidase (GSHPx) and superoxide dismutase (SOD) were analyzed and myocardial tissue was examined histopathologically. Comparisons of groups were done with Kruskal-Wallis one-way analysis test. All pairwise multiple comparisons and the comparisons between control and other groups were done with Dunn's nonparametric multiple comparison test.


RESULTS
Plasma and tissue MDA levels among groups were different (p=0.001 for plasma MDA and p=0.001 for tissue MDA). Plasma MDA levels of HDN, HDNM, LDN, and tissue MDA levels of HDN and LDN were significantly higher than in control group (p<0.05 for plasma MDA and for tissue MDA). Plasma and tissue NO levels among groups were also different (p=0.011 for plasma NO and p=0.001 for tissue NO). Plasma NO of LDN group was higher than of LDNM group, and plasma NO of LDNM group was lower than in control group (p<0.05). Tissue NO levels of HDN and LDN groups were higher than of control group (p<0.05). There was no difference between plasma GSHPx levels among groups (p=0.221) but statistically significant different was detected between tissue GSHPx levels among groups (p=0.001). Tissue GSHPx level was found lower in HDN group than in control group (p<0.05). Tissue GSHPx level of LDNM group was higher than of LDN group, and tissue GSHPx level of HDNM group was higher than of HDN group (p<0.05). A difference was found between plasma and tissue SOD among groups (p=0.005 for plasma SOD and p=0.001 for tissue SOD). Plasma SOD of LDN group was significantly lower than of HDNM and LDNM groups (p<0.05). Tissue SOD analyzes revealed lower levels in HDN and LDN groups than in control group (p<0.05). Severe cardiomyopathy was determined in HDN and LDN groups (p<0.05).


CONCLUSIONS
Nicotine exposure depletes myocardial antioxidant enzymes and increases free radicals and lipid peroxidation products. Melatonin particularly prevents the nicotine-induced cardiac injury as an antioxidant.
Baykan
Ali
A
Department of Pediatrics, Medical Faculty, Erciyes University, Kayseri, Turkey. abaykan@erciyes.edu.tr
Narin
Nazmi
N
Narin
Figen
F
Akgün
Hülya
H
Yavaşcan
Selda
S
Saraymen
Recep
R
D000818:Animals; D000831:Animals, Newborn; D000975:Antioxidants / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005260:Female; D005979:Glutathione Peroxidase / Q000097:blood; D008315:Malondialdehyde / Q000097:blood / Q000378:metabolism; D018811:Maternal Exposure; D008550:Melatonin / Q000494:pharmacology*; D009203:Myocardial Infarction / Q000139:chemically induced / Q000201:enzymology / Q000517:prevention & control*; D009206:Myocardium / Q000201:enzymology*; D009538:Nicotine / Q000633:toxicity*; D009569:Nitric Oxide / Q000097:blood; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced / Q000201:enzymology / Q000517:prevention & control*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000097:blood
D000975:Antioxidants; D009569:Nitric Oxide; D008315:Malondialdehyde; D009538:Nicotine; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D008550:Melatonin