title: Modulatory effects of melatonin and vitamin  C on oxidative stress-mediated haemolytic anaemia and associated cardiovascular dysfunctions in rats.
abstract: Background Phenylhydrazine (PHE) in experimental animal models has been widely reported to cause haemolytic anaemia, via the induction of oxidative stress and thus causing deleterious cardiovascular complications. Hence, this study was designed to evaluate the possible modulatory role of melatonin (MLT) or vitamin C when co-administered with PHE. Methods Anaemia was established with PHE administration. MLT or vitamin C was co-administered with PHE. Haematological parameters, markers of oxidative stress, enzymic and non-enzymic antioxidants, blood pressure and electrocardiograms were assessed. Results PHE administration led to a significant (p<0.05) increase in malondialdehyde (MDA), and hydrogen peroxide (H2O2) generated in cardiac, renal and red blood cell (RBC) lysates. PHE also significantly reduced the activity of glutathione peroxidase (GPx), superoxide dismutase (SOD) and reduced glutathione (GSH) contents, respectively. The RBC counts, haemoglobin (Hb) concentration and packed cell volume (PCV) were also significantly reduced following the administration of PHE. Furthermore, the systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial blood pressure (MABP) increased significantly in rats administered PHE alone. Similarly, PHE administration led to a significant drop in heart rate but prolonged QRS, QT and QTc interval. Pathology of the heart and kidney was also observed in PHE treated group. However, treatment with MLT and vitamin C improved enzymic and non-enzymic antioxidant system together with the restoration of SBP, DBP and MABP to near normal. The architectural anarchy observed in the heart and kidney of PHE administered rats was reversed to some extent. Conclusions Hence, MLT and vitamin C could be employed as therapeutic targets in various cardiovascular diseases and its complications.
authors.forename: Temitayo Olabisi
authors.initials: TO
authors.lastname: Ajibade
authors.forename: Ademola Adetokunbo
authors.initials: AA
authors.lastname: Oyagbemi
authors.forename: Ladoke A
authors.initials: LA
authors.lastname: Durotoye
authors.forename: Temidayo Olutayo
authors.initials: TO
authors.lastname: Omóbòwálé
authors.forename: Ebunoluwa Racheal
authors.initials: ER
authors.lastname: Asenuga
authors.forename: Funsho Olakitike
authors.initials: FO
authors.lastname: Olayemi
mesh_terms: D000743:Anemia, Hemolytic / Q000097:blood / Q000139:chemically induced / Q000150:complications / Q000188:drug therapy*; D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology / Q000627:therapeutic use*; D001205:Ascorbic Acid / Q000494:pharmacology / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects*; D002374:Catalase / Q000378:metabolism; D004912:Erythrocytes / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006321:Heart / Q000187:drug effects; D006454:Hemoglobins / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000097:blood; D006973:Hypertension / Q000097:blood / Q000209:etiology / Q000517:prevention & control*; D007668:Kidney / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008550:Melatonin / Q000494:pharmacology / Q000627:therapeutic use*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects*; D010659:Phenylhydrazines; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D014815:Vitamins / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D000975:Antioxidants; D006454:Hemoglobins; D010659:Phenylhydrazines; D014815:Vitamins; C030299:phenylhydrazine; D008315:Malondialdehyde; D006861:Hydrogen Peroxide; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione; D008550:Melatonin; D001205:Ascorbic Acid