The aim of the present study was to investigate the ameliorative effect of curcumin (CMN) against acute cadmium chloride (CdCl(2)) toxicity on male reproductive system in rats. CdCl(2) is known to be a heavy metal and potential environmental pollutant. For this purpose, 28 rats were equally divided into four groups; the first group was kept as control and given distilled water and corn oil as carrier. In second and third groups, CdCl(2) and CMN were administered at the dose with 1 mg kg(-1) day(-1) and 100 mg kg(-1) for 3 days respectively. CdCl(2) and CMN were given together at the same doses in the fourth group. It was determined that acute CdCl(2) exposure caused a significant reproductive damage via increased oxidative stress (increased TBARS levels and decreased SOD, CAT, GPx and GSH levels), histological alterations (necrosis, oedema etc.) and spermatological damage (decreased sperm motility and sperm concentration and increased abnormal sperm rate) in male rats. However, CMN treatment partially reversed these toxic effects of CdCl(2) on the reproductive system. In conclusion, our results show that acute exposure of CdCl(2) may lead to infertility, and CMN could prevent and reverse hazardous effects of CdCl(2) to some degree. Thus, CMN may be useful for the prevention of CdCl(2)-induced reproductive damage.

2,3,7,8-Tetracholorodibenzo-p-dioxin (TCDD) is a highly toxic environmental contaminant that causes severe toxic effects in animal and human. In this study, we investigated the toxic effects of TCDD and the preventive effects of protocatechuic acid (PCA), a widespread phenolic compound, in the heart tissue of rats. For this purpose, 3-4 months old 28 rats with 280-310 g body weights were equally divided into 4 groups (control, TCDD, PCA, TCDD + PCA group). A 2 μg/kg dose of 2,3,7,8-TCDD and 100 mg/kg dose of PCA were dissolved in corn oil and given orally to the rats for 45 days. The results indicated that TCDD induced oxidative stress by increasing the level of thiobarbituric acid reactive substance and by decreasing the levels of glutathione, catalase, glutathione peroxidase and superoxide dismutase in the heart tissue of rats. In contrast, PCA treatment prevents the toxic effects of TCDD on oxidative stress. In addition, histopathological alterations such as necrosis and hemorrhage occurred in TCDD group, and PCA treatment partially prevents these alterations in heart tissue. In this study, it was concluded that TCDD exposure led to toxic effects in heart tissue and PCA treatment could prevent the toxicity of TCDD.

In this study, it was aimed to determinate beneficial effects of protocatechuic acid (PCA) against reproductive toxicity caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an environmental contaminant. For this purpose, 28 rats were equally divided into four groups (control, TCDD 2 μg kg(-1) per week, PCA 100 mg kg(-1) per day and TCDD + PCA group), and compounds were orally administered for 45 days. The results indicated that TCDD induced oxidative stress via an increase in thiobarbituric acid-reactive substances levels and a decrease in reduced glutathione, catalase, glutathione peroxidise and SOD levels in male rats. In contrast, PCA treatment prevented toxic effects of TCDD in terms of oxidative stress. Additionally, sperm motility, sperm concentration and serum testosterone levels significantly decreased, and pathologic testicular damage increased with TCDD exposure. However, these effects of TCDD on sperm characteristics, histopathological changes and hormone levels were reversed by PCA treatment. In conclusion, it was found that TCDD exposure induced reproductive toxicity (oxidative, hormonal, histopathological and spermatological alternations) in male rats and PCA treatment could prevent toxic effects of TCDD. Thus, PCA may be useful for the prevention and treatment of reproductive toxicity caused by TCDD.

Fifteen bald eagles (Haliaeetus leucocephalus) and 3 golden eagles (Aquila chrysaetos) were diagnosed with West Nile disease based on 1) presence of lesions in brain, eyes, and heart, 2) viral antigen detection in brain, eyes, heart, kidney, and/or liver by immunohistochemical staining, 3) detection of viral RNA in tissue samples and/or cerebrospinal fluid (CSF) by polymerase chain reaction, and/or 4) detection of West Nile virus (WNV)-specific antibodies in CSF by serum neutralization assay. West Nile virus-associated gross lesions included cerebral pan-necrosis with hydrocephalus ex vacuo (7/15 bald eagles), fibrin exudation into the fundus in 1 golden eagle, retinal scarring in 1 bald eagle, and myocardial pallor and rounded heart apex in 4 bald eagles. Histologic lesions included lymphoplasmacytic encephalitis, most prominently in the cerebrum (17 eagles), lymphoplasmacytic pectenitis and choroiditis (15 and 8 eagles, respectively), and myocarditis (12 eagles). West Nile virus antigen was detected in the majority of the eagles in neurons of the brain (cerebrum and cerebellum), and less commonly present in neurons of the retina, tubular epithelial cells of the kidney, and cardiomyocytes. West Nile disease was diagnosed in 2 bald eagles based on the presence of cerebral pan-necrosis and WNV-specific antibodies in the CSF despite lacking viral antigen and RNA. In conclusion, WNV infection causes a fatal disease in bald and golden eagles. A variety of gross and histologic lesions are highly suggestive of WN disease in most eagles. A combination of detection of viral antigen and/or RNA or virus-specific antibodies proved useful in confirming the diagnosis.