Gunes, SibelSahinturk, VarolKarasati, PinarSahin, Ilknur KulcanayAyhanci, Adnan2020-06-252020-06-252017closedAccess0163-49841559-0720https://doi.org/10.1007/s12011-016-0858-1https://hdl.handle.net/20.500.12587/6992Gunes, Sibel/0000-0003-0846-1170; Sahinturk, Varol/0000-0003-2317-3644The objective of this study is to evaluate the possible protective effects of selenium (Se) against cyclophosphamide (CP)-induced acute cardiotoxicity in rats. A total of 42 male Spraque-Dawley rats were divided into six groups (n = 7). Rats in the first group were served as control. Rats in the second group received CP (150 mg/kg) at the sixth day of experiment. Animals in the third and fourth groups were treated with only 0.5 and 1 mg/kg Se respectively for six consecutive days. Rats in the fifth and sixth groups received respective Se doses (0.5 or 1 mg/kg) for 6 days and then a single dose of CP administered on the sixth day. On day 7, the animals were sacrificed; blood samples were collected to measure malondialdehyde (MDA), glutathione (GSH), lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), and ischemia-modified albumin (IMA) levels. Heart tissues were processed routinely and tissue sections were stained with H + E for light microscopic examination. In the CP-treated rats MDA, LDH, CK-MB, and IMA serum levels increased, while GSH levels decreased. Microscopic evaluation showed that tissue damage was conspicuously lower in CP plus Se groups. Moreover, 1 mg/kg Se was more protective than 0.5 mg/kg Se as indicated by histopathological and biochemical values. In conclusion, Se is suggested to be a potential candidate to ameliorate CP-induced cardiotoxicity which may be related to its antioxidant activity.eninfo:eu-repo/semantics/closedAccessCyclophosphamideOxidative stressCardiotoxicitySeleniumIschemia modified albuminArticle177110711410.1007/s12011-016-0858-12-s2.0-8499081836227709497Q1WOS:000398712400014Q3