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Background: Human exposure to cyclophosphamide (CP) is highly frequent because it is widely used chemotherapeutic and immunosuppressive. CP has potential toxic effects on liver and kidney that make it an issue of concern to public health. Selenium (Se) is an essential dietary element with a high nutritional value, immunomodulatory and antioxidant properties. This study aimed to evaluate the protective role of Se against toxic effects of CP in hepatic and renal tissues of adult male albino rats. Methods: The study was carried on 42 adult male albino rats were divided into 6 groups, 7 rats for each group. Group I (Negative control). group II (Positive control): divided into group IIA (Distilled water), group IIB (Normal saline), group III (Selenium), group IV (CP) and group V (CP + Se). The following markers were measured: serum ALT (Alanine aminotransferase), AST(Aspartate transaminase), LDH (Lactate dehydrogenase), Urea and Creatinine. Hepatic and renal tissue MDA (Malondialdehyde), PCC (Protein carbonyl content), catalase, GSH (Reduced glutathione) and IL-6 (Interleukin six). Histopathological and Immunohistochemical staining studies were demonstrated. Results: In CP administrated rats, serum ALT, AST, LDH, Urea and Creatinine levels increased. Also, CP induced elevation in hepatic and renal tissues MDA, PCC and IL-6 and a decrease in hepatic and renal tissues catalase and GSH. Histopathology and Immunohistochemical staining showed that: CP induced histological damages and strong immunoreaction decreased by cotreatment of Se. Conclusion: Administration of Se improved liver and kidney functions and histology beside improvement in oxidative stress and inflammation caused by CP. [ABSTRACT FROM AUTHOR]

ABSTRACT Alpha-cypermethrin (α-CYP) is one of the most widely used insecticides. It may become an air pollutant and adversely affect the health. The present study was designed to determine whether treatment with N-acetyl cysteine (NAC), a well-known antioxidant, can be useful for the management of the deleterious effects of α-CYP on lung tissues. For this purpose, thirty two male rats were divided into four different groups (eight rats for each). Group (I) gavaged with corn oil (control group), group (II) gavaged daily with NAC (150 mg kg−1 body weight), group (III) gavaged with α-CYP (14.5 mg kg−1 body weight/day, dissolved in corn oil), group (IV) gavaged with NAC then with α-CYP 2 h later for 12 weeks. α-CYP significantly increased serum lactate dehydrogenase (LDH) and pulmonary malondialdehyde (MDA) levels, while decreased the activities of catalase (CAT) and superoxide dismutase (SOD) as well as reduced glutathione (GSH) content in lung. It also provoked higher levels of serum nitric oxide (NO), lung interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), hydroxyproline (Hyp) as well as heme oxygenase-1 (HO-1), inducible nitric oxide synthase (iNOS) and nuclear factor-kappa B (NF-КB) gene expression in lung tissues. Histopathological alterations in lung with congestion, cellular infiltration, necrotic changes and thickening of inter-alveolar septa were observed following α-CYP administration. NAC reduced the adverse effects of α-CYP on lung tissues and improved the histological architecture of lung since it showed antioxidant, anti-inflammatory and antifibrotic effects on lung tissues. Our results indicate that NAC exerts a potent protective effect against α-CYP-induced oxidative damage and inflammation in lung tissues. © 2013 Wiley Periodicals, Inc. Environ Toxicol 30: 26-43, 2015. [ABSTRACT FROM AUTHOR]