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This study investigated the potential p-chloro-selenosteroid (PCS) anti-inflammatory effect in different animal models of acute inflammation. In order to determine a time- and a dose-curve response of action, female adult Swiss mice (25-35g) were divided in different groups and pretreated by the intragastric route (i.g.) with PCS (5-10mg/kg) and after the specific times (5, 30 and 60min) the ear inflammation was induced with croton oil (2.5%, 20μl). The ear edema, myeloperoxidase (MPO) activity and histological analyses were performed. In a second experiment, the pleurisy model was used to determine the PCS protective effect (10mg/kg, i.g., 30min before induction) in the inflammatory and oxidative alterations induced by an intrapleural injection of a 1% carrageenan solution (0.1ml) in exudate and lung samples. Dexamethasone (1mg/kg, i.g.) was used as positive control for both models. Statistical analysis was performed through a One-Way ANOVA test followed by the Newman-Keuls' test. Pretreatment of 30min with PCS, only at a dose of 10mg/kg, decreased ear edema and the MPO activity as well as the histological alterations induced by croton oil. In the pleurisy model, PCS (10mg/kg, i.g.; 30min) reduced the leukocyte counts, histological alterations, MPO and adenosine deaminase activities, oxidative damage and the non-enzymatic antioxidant defense imbalance. PCS had a similar anti-inflammatory profile to dexamethasone; however, it showed a better antioxidant effect. PCS had anti-inflammatory and antioxidant actions in two well established inflammation models in mice., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Diminazene aceturate (DA) is the active component of some trypanocidal drugs used for the treatment of animals infected with trypanosomosis and babesiosis. Residues of DA may cause hepatotoxic and nephrotoxic effects. Therefore, the purpose of this study was to investigate the occurrence of oxidative stress, i.e., changes in the antioxidant defense system of rats treated with a single dose of 3.5 mg kg(-1) of DA. All treatments were intramuscularly administered, and evaluations were performed on days 7 and 21 post-treatment (PT). Liver and kidney samples were collected and evaluated by histopathology and oxidative stress parameters (thiobarbituric acid-reactive species, catalase, superoxide dismutase, carbonyl, non-protein thiols, and reduced glutathione). Finally, blood was collected to determine seric DA concentration. Superoxide dismutase (SOD) and catalase (CAT) activities in liver and kidney of rats were dramatically inhibited (p < 0.05) compared to the control group on day 21 PT. This difference is related to the concomitant increase (p < 0.05) in malondialdehyde (MDA) content, which was identified by an increase in thiobarbituric acid-reactive species (TBARS) levels. The carbonyl levels did not differ between groups (p > 0.05). Both non-protein thiols (NPSH) and glutathione (GSH) levels in liver and kidney decreased (p < 0.05) on day 21 PT. Chromatographic analyses showed lower levels of DA on day 21 PT compared to day 7 PT. A negative correlation was observed between DA concentration in serum and lipid peroxidation in liver and kidney tissues on 21 days PT. Histopathology revealed vacuolar degeneration in liver and kidney samples on day 21 PT. Our findings indicate that DA could cause oxidative damage to liver and kidney of rats.

The aim of the present study was to evaluate the possible effects of zinc chloride against the gastrointestinal lesions caused by oral administration of ethanol in rats. Rats were divided into five groups, namely, saline, ethanol, zn, zn+ethanol and ethanol+zn. Ethanol 70% (2 mL/kg) was administered by gavage in 36 h fasted rats. Zinc chloride (27 mg/kg, ~13 mg/kg of zinc) was given by gavage 1h before or 1h after the administration of ethanol. Oral administration of ethanol consistently induced damage in the rat glandular stomach and intestine. Zinc did not demonstrate effect per se and significantly reduced gastrointestinal lesions when administered either before or after lesion induction. Ethanol induced enhancement of thiobarbituric acid reactive substance and reactive species levels, diminished the ascorbic acid and total protein SH content as well as superoxide dismutase and catalase activity in stomach and intestine of rats. Zinc treatment prevented and reversed these alterations induced by ethanol. Stomach and intestine of rats treated with zinc presented higher zinc content than the tissues of rats treated only with ethanol. Non-protein SH content was not altered by any treatment. Results suggested that the gastrointestinal protective effect of zinc in this experimental model could be due to its antioxidant effect., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Acetaminophen (APAP) hepatotoxicity has been related to several cases of hepatitis, cirrhosis, and hepatic transplant. As APAP hepatotoxicity is related to reactive oxygen species (ROS) formation and excessive oxidative stress, natural antioxidant compounds have been tested as an alternative therapy to diminish the hepatic dysfunction induced by APAP. Taraxacum officinale Weber (Family Asteraceae), commonly known as dandelion, is used for medicinal purposes because of its choleretic, diuretic, antioxidant, anti-inflammatory, and hepatoprotective properties. This study evaluated the hepatoprotective activity of T. officinale leaf extract against APAP-induced hepatotoxicity. T. officinale was able to decrease thiobarbituric acid-reactive substance levels induced by 200 mg/kg APAP (p.o.), as well as prevent the decrease in sulfhydryl levels caused by APAP treatment. Furthermore, histopathological alterations, as well as the increased levels of serum aspartate and alanine aminotransferases caused by APAP, were prevented by T. officinale (0.1 and 0.5 mg/mL). In addition, T. officinale extract also demonstrated antioxidant activity in vitro, as well as scavenger activity against 2,2-diphenyl-1-picrylhydrazyl and nitric oxide radicals. Our results clearly demonstrate the hepatoprotective effect of T. officinale against the toxicity induced by APAP. The possible mechanisms involved include its scavenger activities against ROS and reactive nitrogen species, which are attributed to the content of phenolic compounds in the extract.