Protective effects of melatonin against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced cardiac injury in rats.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is the prototype of a group of highly toxic environmental chemicals. Although there are some suggestions regarding TCDD-induced cardio-toxicity, the exact mechanisms underlying this process have not been fully discovered. One mechanism related to this toxicity is believed to be the generation of reactive oxygen species. Melatonin is known to be a strong antioxidant and has a free radical scavenging ability. Therefore, the aim of this study was to investigate the TCDD-induced cardio-toxicity and the protective effects of melatonin in rats. Rats were randomly divided into 4 equal groups (n=7 for each group). Group 1 was control; group 2 was TCDD group (2µg/kg/week, p.o); group 3 was melatonin group (5mg/kg/day, i.p.) and group 4 was TCDD and melatonin treatment group. All agents were continued to be administered until the 45th day. Body/heart weights, mean oxygen saturation (PO2%), hemodynamic [mean blood pressure (MBP) and heart rate (HR) from the cannulated-carotid artery] and electrocardiographic evaluations (arrhythmias and duration of PR, QRS and QT intervals), biochemical and histopathological analysis were carried out. TCDD exposure caused significant body and heart weight loss, impairment of PO2%, and decrease of MBP and HR levels. Also, major ECG changes and prolongation of PR, QRS and QT durations were observed in TCDD-exposed rats. In biochemical analysis, TCDD significantly induced lipid peroxidation and reduced antioxidant activities. Moreover, our histopathological observations were in accordance with the biochemical results. According to the results, melatonin treatment significantly protected the subjects from TCDD-induced cardio-toxicity.

Pathological and immunohistochemical findings in broilers inoculated with a low virulent strain of infectious laryngotracheitis virus.

This study was carried out to describe clinical, gross and histopathological findings in the respiratory tract in chickens infected intranasally with A96 strain of infectious laryngotracheitis virus (ILTV). In addition, the presence of ILTV antigens in formalin-fixed and paraffin-embedded larynx and trachea tissues was investigated with the immunoperoxidase (IP) method in the infected chickens. At various days of viral infection, nares, larynx, trachea, lungs and air sacs tissue samples of the infected chickens were obtained and fixed with formalin and embedded in paraffin. The cross sections were stained with hematoxylineosin, and the larynx and trachea sections were also stained with the IP method. Mild rales and gasping were observed in only 4 of 35 chickens. The virus caused mild inflammatory changes in the respiratory tract. It was shown that clinical, gross and histopathological findings were not specific for differential diagnosis of the disease. However, ILTV antigens were detected by the IP method in formalin-fixed and paraffin-embedded larynx and trachea sections. These results revealed that the study use of the IP method might be useful for the diagnosis of ILTV infections with non-specific lesions.

Montelukast attenuates side effects of cisplatin including testicular, spermatological, and hormonal damage in male rats.

In the current study, the protective effect of montelukast (ML) on cisplatin induced reproductive toxicity in rats was investigated. Twenty-eight rats were equally divided into four groups; first group was kept as control. In the second group, ML was orally administered at the dose of 10 mg/kg/day for 10 days. In the third group, CP was intraperitoneally administered at the dose of 7 mg/kg a single injection, and in fourth group, CP and ML were given together at the same doses. Although CP induced oxidative stress via significant increase in the formation of TBARS, it caused a significant decline in the levels of GSH, CAT, GPx, and SOD in rats. In contrast, ML prevents these effects of CP through cause an increase in GSH, CAT, GPx, and SOD levels and a decrease in formation of TBARS. In addition, sperm motility and serum testosterone levels significantly decrease and histopathological damage increases with CP treatment. However, the effects of CP on sperm motility, serum testosterone level, oxidative and histopathological changes are eliminated by ML treatment. In conclusion, the current study demonstrated that the reproductive toxicity caused by CP may be prevented by ML treatment. Thus, it was judged that co-administration of ML with CP may be useful to attenuate the negative effects of CP on male reproductive system.