In this study, we aimed to evaluate whether edaravone (EDA) has a protective role against valproic acid (VPA)-induced lung damage via its antioxidative activity. Male Sprague-Dawley rats were split into four groups. Control (n = 8) rats; rats given EDA (30 mg kg −1 day −1 ; n = 10); rats given only (VPA, 500 mg kg −1 day −1 ; n = 10); rats given VPA + EDA (in the same dose and time) for 7 days. EDA and VPA were applied intraperitoneally. After 8 days, lung tissues were immediately taken from the rats. In lung homogenates, reduced glutathione, total antioxidant status levels, and superoxide dismutase, glutathione peroxidase, sodium/potassium ATPase, paraoxonase1, and carbonic anhydrase activities significantly abated, whereas catalase, glutathione reductase, glutathione-S-transferase activities insignificantly decreased in the VPA-treated group. In contrast, lipid peroxidation, reactive oxygen species, and total oxidant status levels, glycoprotein and protein carbonyl contents, nitric oxide, hydroxyproline levels, and xanthine oxidase, lactate dehydrogenase, arginase, and prolidase activities significantly increased in the VPA-given group. Administration of EDA caused the reverse effects. As a consequence, EDA prevented oxidative stress-mediated lung injury via its robust antioxidant effects.

Valproic acid (VPA) is a well-established anticonvulsant drug that has been increasingly used in the treatment of many forms of generalized epilepsy. Edaravone (EDA, 3-methyl-1-phenyl-2-pyrazolin-5-one) is a potent free radical scavenger. In this study, the aim was to investigate the effects of EDA on VPA-induced hepatic damage. Male Sprague Dawley rats were divided into four groups. Group I was control animals. Group II was control rats given valproic acid (500 mg kg -1 day -1 ) for seven days. Group III was given only EDA (30 mg kg -1 day -1 ) for seven days. Group IV was given VPA+EDA (at the same dose and in the same time). EDA and VPA were administered intraperitoneally. On the 8 th day of the experiment, blood samples and liver tissue were taken. Serum aspartate and alanine aminotransferase, alkaline phosphatase and bilirubin levels, liver myeloperoxidase, xanthine oxidase, adenosine deaminase, Na + /K + ATPase, sorbitol dehydrogenase, glutamate dehydrogenase, DT-diaphorase, arginase and thromboplastic activities, lipid peroxidation, protein carbonyl levels were increased whereas paraoxonase and biotinidase activities and glutathione levels were decreased in the VPA group. Application of EDA with VPA protected against VPA-induced effects. These results demonstrated that administration of EDA is potentially beneficial to reduce hepatic damage in VPA-induced hepatotoxicity, probably by decreasing oxidative stress.

Hereditary diseases cause yield and economic loses. It is important to examine hereditary diseases at the molecular level and to remove diseases from the herd. In our study, it was aimed to determine allele frequencies of genes that cause bovine leukocyte adhesion deficiency, factor XI deficiency and complex vertebral malformation diseases in Holstein cattle. Blood samples were randomly taken from 300 Holstein cattle in different dairy farms in Kocaeli, Sakarya and Balıkesir provinces. Deoxyribonucleic acid samples were isolated from blood samples by using the standard ammonium acetate salt-out method. The target regions were amplified by polymerase chain reaction to determine the mutant alleles causing bovine leukocyte adhesion deficiency, factor XI deficiency and complex vertebral malformation. According to the nucleotide chromotograms of the samples subjected to bovine leukocyte adhesion deficiency analysis, it was determined that 4 out of 300 cattle were heterozygous and 296 were homozygous. Polymerase chain reaction procedure for factor XI deficiency disease was sufficient, while samples amplified by polymerase chain reaction for complex vertebral malformation disease were subjected to restriction particle length polymorphism. Factor XI deficiency and complex vertebral malformation disease genes were all homozygous normal.

Valproic acid (n-dipropyl-acetic acid, VPA) is a medication used as anticonvulsant in the treatment of bipolar disorder, and for migraine prophylaxis. Long-term use of VPA is known to trigger reproductive impairment, which is mediated by elevation of testicular oxidative stress. Edaravone is used in the treatment of cerebrovascular diseases. It can diffuse into many disease-affected organs, thus shows protective effects in numerous tissues including the heart, lung, and testis. The main goal of the present study was to determine the possible protective role of edaravone against VPA-induced oxidative testicular injury. Male Sprague Dawley rats were assigned into four groups. Control rats; rats given only edaravone (30 mg/kg/day); rats given only VPA (500 mg/kg/day); rats given VPA+edaravone for seven days. Edaravone and VPA were applied intraperitoneally. After eight days, testicular tissues were taken from rats. There was a statistically significant increase in the levels of reduced glutathione, lipid peroxidation, reactive oxygen species, total oxidant status, oxidative stress index, and DNA contents as well as catalase, superoxide dismutase, glutathione-related enzymes, gamma-glutamyl transferase, acid and alkaline phosphatases, lactate dehydrogenase, myeloperoxidase and sorbitol dehydrogenase activities in VPA group. More so, advanced oxidized protein products, protein carbonyl, and nitric oxide levels were also significantly increased in VPA group. Activities of glucose-6phosphate dehydrogenase and sodium/potassium ATPase and total antioxidant status levels remarkably decreased in VPA given group. Treatment with edaravone to VPA group significantly reverted these alterations. These findings demonstrate that administration of edaravone has a beneficial effect against testicular injury in VPA-induced oxidative stress.

Growth and meat production traits are very important in sheep breeding. Cyp19 gene has a major role in reproductive activity and growth due to its function in estrogen synthesis. Another gene affecting growth traits is  Myostatin (MSTN) gene, which mainly regulates skeletal muscle growth. In this study allele frequencies of genetic polymorphism in Cyp19 and Myostatin genes were identified by PCR-RFLP method in five indigenous Turkish sheep breeds, Chiose, Imroz, Kivircik, Zom and Morkaraman. Digestion of Cyp19 gene with HaeIII only revealed uncut AA genotype and digestion of MSTN with DraI also revealed only uncut AA genotype. Both loci analyzed in this study were found to be monomorphic in five Turkish indigenous sheep breeds. These highly conserved parts of the two genes can be useful for molecular evolutionary studies in sheep. Further studies regarding association analysis of Cyp19 and MSTN in sheep should be conducted.