Antioxidant role of selenium against maneb-induced cardiotoxicity in mice.

The current study was conducted to assess the beneficial effect of selenium (Se) on maneb-induced cardiotoxicity and fatty acid alterations in adult mice. Swiss albino male mice were assigned into four experimental groups. The first group consisted of negative controls. The second group represented the positive controls where mice received daily, via the diet, sodium selenite at a dose of 0.2 mg/kg. For the third group, mice were subjected to intraperitoneal injections of maneb (30 mg/kg BW). The fourth group (MB+Se) received daily the same dose of maneb as group 3 along with sodium selenite at the same dose as group 2. Mice exposure to maneb caused cardiotoxicity as indicated by an increase in malondialdehyde, hydrogen peroxide, and protein carbonyl levels, and an alteration of the antioxidant defense system (catalase, glutathione peroxidase, superoxide dismutase, glutathione, and vitamin C). Plasma lactate dehydrogenase activity and total cholesterol, triglyceride, and low-density lipoprotein cholesterol levels increased, while high-density lipoprotein cholesterol level decreased. Results showed also a decrease in the amount of n-3 PUFA, docosahexaenoic, docosapentaenoic, and eicosapentaenoic acids. However, an increase in the levels of MUFA, cis-vaccenic, and palmitoleic acids was observed. Co-administration of Se restored the parameters indicated above to near control values. The histopathological findings confirmed the biochemical results. Selenium could be a useful and efficient agent against maneb-induced cardiotoxicity.

Ovarian Steroid Cell Tumor (Not Otherwise Specified): A Case Report of Ovarian Hyperandrogenism.

Steroid cell tumors (SCTs) (not otherwise specified (NOS)) are rare sex cord-stromal tumors of the ovary. These are associated with hormonal disturbances resulting in menstrual bleeding patterns and androgenic effects. We report the case of a 36-year-old female presented with hirsutism, signs of virilization, and elevated androgen levels. Transvaginal ultrasound showed a solid-appearing right ovarian mass. She underwent fertility-sparing surgery with a laparoscopic left oophorectomy. Histological examination showed a benign steroid cell tumor, NOS. These tumors often small can then present a problem of positive diagnosis responsible for a delay in the diagnosis.

Nitrate-induced biochemical and histopathological changes in the liver of rats: ameliorative effect of Hyparrhenia hirta / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>The present study investigated the protective role of Hyparrhenia hirta (H. hirta) against sodium nitrate (NaNO3)-induced hepatoxicity.</p><p><b>METHODS</b>Male Wistar rats were randomly divided into three groups: a control group and two treated groups during 50 d with NaNO3 administered either alone in drinking water or co-administered with H. hirta.</p><p><b>RESULTS</b>NaNO3 treatment induced a significant increase in serum levels of glucose, total cholesterol and triglyceride while serum total protein level decreased significantly. Transaminases and lactate deshydrogenase activities in serum were elevated indicating hepatic cells' damage after treatment with NaNO3. The hyperbilirubinemia and the increased serum gamma glutamyl transferase activities suggested the presence of cholestasis in NaNO3 exposed rats. In parallel, a significant increase in malondialdehyde level along with a concomitant decrease in total glutathione content and superoxide dismutase, catalase and glutathione peroxidase activities were observed in the liver after NaNO3 treatment. Furthermore, nitrate caused a significant induction of DNA fragmentation. These modifications in NaNO3-treated rats corresponded histologically with hepatocellular necrosis and mononuclear cells infiltration. H. hirta supplementation showed a remarkable amelioration of the abnormalities cited above.</p><p><b>CONCLUSION</b>The results concluded that the treatment with H. hirta had a significant role in protecting the animals from nitrate-induced liver dysfunction.</p>

Dimethoate induced oxidative damage and histopathological changes in lung of adult rats: modulatory effects of selenium and/or vitamin E / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To determine the efficiency of selenium and/or vitamin E to alleviate lung oxidative damage induced by dimethoate, an organophosphorus compound.</p><p><b>METHODS</b>Adult Wistar rats were exposed during 30 days either to dimethoate (0.2 g/L of drinking water), dimethoate+selenium (0.5 mg/kg of diet), dimethoate+vitamin E (100 mg/kg of diet), or dimethoate+selenium+vitamin E.</p><p><b>RESULTS</b>Exposure to dimethoate caused oxidative stress in lung evidenced by an increase of malondialdehyde, protein carbonyl groups and advanced oxidation protein products. An increase in glutathione peroxidase, superoxide dismutase, catalase and a decrease in acetylcholinesterase and butyrylcholinesterase activities, glutathione, non-protein thiols and vitamins C levels were observed. Histopathological changes in lung tissue were noted as emphysema, hemorrhages and hemosiderin deposits. Co-administration of selenium or vitamin E to the diet of dimethoate treated rats ameliorated the biochemical parameters as well as histological impairments. The joint effect of these elements was more powerful in antagonizing dimethoate-induced lung oxidative damage.</p><p><b>CONCLUSION</b>We concluded that selenium and vitamin E ameliorated the toxic effects of this pesticide in lung tissue suggesting their role as potential antioxidants.</p>

Hepatoid adenocarcinoma of the gallbladder.

Hepatoid adenocarcinoma is a rare variant of extrahepatic adenocarcinoma which behaves like hepatocellular carcinoma in morphology and functionality. We present a rare case of hepatoid adenocarcinoma of the gallbladder which invades deeply the liver bed, in a 59-year-old woman. Histologically, most of the mass in the gallbladder was composed of cells with eosinophilic cytoplasm arranged in a trabecular pattern, which resembled hepatocellular carcinoma. The main differential diagnosis was hepatocellular carcinoma with invasion into the gallbladder. The gallbladder origin of the hepatoid adenocarcinoma was verified by the presence of foci of conventional adenocarcinoma, the recognition of high-grade dysplasia in the adjacent epithelium and the absence of cirrhosis.