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OBJECTIVES: S-methyl cysteine sulfoxide (SMCS) is a hydrophilic cysteine-containing natural compound found in plants and is known to possess antidiabetic and antioxidant properties. We investigated the antioxidant and immunomodulatory properties of SMCS, as well as histopathological changes in the liver and pancreas in streptozotocin (STZ)-induced diabetic rats. METHODS: The rats were divided into the following groups: control (CG), comprising non-diabetic rats; STZ-DB, comprising STZ-induced diabetic rats; and STZ-SMCS, comprising STZ-induced diabetic rats treated with SMCS. SMCS (200 mg/kg) was administered by gavage daily for 30 days. Biochemical and cytokine analyses, catalase (CAT) and superoxide dismutase (SOD) activities assays and histopathological analysis of liver and pancreas tissues were performed. RESULTS: SMCS treatment reduced glycemia (p<0.05), decreased triglyceride (p<0.01) and very-low-density lipoprotein (VLDL) levels (p<0.01), and increased SOD and CAT activity in the liver (both p<0.01) compared with STZ-DB group. Higher activity values of IL-10 were observed in the STZ-SMCS group than in the other groups (p<0.001). Liver glycogen was significantly improved in the STZ-SMCS group compared with the STZ-DB group. SMCS also ameliorated damage to pancreatic islets, which resulted in restoration of their morphology. CONCLUSIONS: Oral treatment of SMCS showed improvement of the morphological alterations in liver and pancreatic islet in diabetic rats. These beneficial morphological effects of SMCS can be partially explained by IL-10 modulation associated with antioxidant action.

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Background: Hyperbaric oxygen (HBO2) is currently emerging as a promising therapeutic option for diseases involving impaired tissue repair and remodeling. In this regard, HBO2 has been shown to modulate signaling pathways responsible for matrix metalloproteinases (MMPs) regulation, which makes the MMPs interesting targets for investigation. However, the understanding regarding how HBO2 treatment affects the expression and activity of the MMP family members in different tissues and diseases needs to be clarified. The precise roles of MMPs in the physiopathology of various tissue repair disorders also remain unclear. Because of potential off-target systemic effects of the HBO2 on MMPs, researchers and physicians should carefully consider whether their patients could be affected adversely by HBO2 exposure. Aims: This narrative review provides an overview of MMP biology (structure, function, and regulation) and summarizes available data showing how MMPs respond to HBO2 in different tissues and pathologies, also highlighting possible mechanisms.

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The aim of the present study was to investigate the activities of natural chondroitin sulfates (CS) with different structures on cultured chondrocytes and macrophages. CS were isolated from cartilages of bovine trachea (BT), porcine trachea (PT), chicken sternum (Ch) and skate (Sk). The preparations were 90-98% pure, with ∼1% proteins, nucleic acids and keratan sulfate contaminants. Structural analysis of these CS and of commercial chondroitin 4- and 6-sulfate (C4S, C6S) have shown that most of their disaccharides are monosulfated, with varying proportions of 4- and 6-sulfation, and 2-7% non-sulfated disaccharides. Sk-CS and C6S contained detectable amounts of disulfated disaccharides. All the CS were polydisperse, with modal molecular weights of 26-135kDa. These CS had anti-inflammatory activities on both chondrocytes and macrophages, but with different efficiencies. On horse and human chondrocytes, they reduced the IL-1ß-induced liberation of NO and PGE2, and on RAW 264.7 immortalized macrophage-like cell line, C4S, C6S, Ch and Sk-CS decreased the LPS-induced liberation of TNF-α, but did not affect IL-6. In contrast, on bone marrow derived macrophages, C4S, C6S, BT and PT-CS reduced the LPS-induced liberation of TNF-α, IL-6, IL-1ß and NO, indicating that the RAW response to CS was different from that of primary macrophages.

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Emerging contaminants including pharmaceuticals are a class of compounds that are causing great concern due to several environmental problems. Conventional water and wastewater treatments do not achieve high removal efficiencies for many of these drugs. Therefore, the present work investigated the removal of ibuprofen (IBP) by heterogeneous photocatalysis using TiO2 irradiated with artificial UV light or solar radiation. The treated solutions were tested against Daphnia similis and Raphidocelis subcapitata, which are species commonly used as bioindicators of environmental conditions. The results indicated that IBP removal reached 92% after 1 h of treatment using artificial UV and 1000 mg L-1 of TiO2, which was the optimum catalyst concentration in the range studied (20-1000 mg L-1). TOC removal reached up to 78% after 60 min of treatment using TiO2/artificial UV. Ecotoxicological bioassays indicated that the treated solutions had acute effects, with 30% immobilization of D. similis and 40% growth inhibition of R. subcapitata.

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Emerging contaminants including pharmaceuticals are a class of compounds that are causing great concern due to several environmental problems. Conventional water and wastewater treatments do not achieve high removal efficiencies for many of these drugs. Therefore, the present work investigated the removal of ibuprofen (IBP) by heterogeneous photocatalysis using TiO2 irradiated with artificial UV light or solar radiation. The treated solutions were tested against Daphnia similis and Raphidocelis subcapitata, which are species commonly used as bioindicators of environmental conditions. The results indicated that IBP removal reached 92 % after 1 h of treatment using artificial UV and 1000 mg L(-1) of TiO2, which was the optimum catalyst concentration in the range studied (20-1000 mg L(-1)). TOC removal reached up to 78 % after 60 min of treatment using TiO2/artificial UV. Ecotoxicological bioassays indicated that the treated solutions had acute effects, with 30 % immobilization of D. similis and 40 % growth inhibition of R. subcapitata.

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Analysis of fuel emissions is crucial for understanding the pathogenesis of mortality because of air pollution. The objective of this study is to assess cardiovascular and inflammatory toxicity of diesel and biodiesel particles. Mice were exposed to fuels for 1 h. Heart rate (HR), heart rate variability, and blood pressure were obtained before exposure, as well as 30 and 60 min after exposure. After 24 h, bronchoalveolar lavage, blood, and bone marrow were collected to evaluate inflammation. B100 decreased the following emission parameters: mass, black carbon, metals, CO, polycyclic aromatic hydrocarbons, and volatile organic compounds compared with B50 and diesel; root mean square of successive differences in the heart beat interval increased with diesel (p < 0.05) compared with control; low frequency increased with diesel (p < 0.01) and B100 (p < 0.05) compared with control; HR increased with B100 (p < 0.05) compared with control; mean corpuscular volume increased with B100 compared with diesel (p < 0.01), B50, and control (p < 0.001); mean corpuscular hemoglobin concentration decreased with B100 compared with B50 (p < 0.001) and control (p < 0.05); leucocytes increased with B50 compared with diesel (p < 0.05); platelets increased with B100 compared with diesel and control (p < 0.05); reticulocytes increased with B50 compared with diesel, control (p < 0.01), and B100 (p < 0.05); metamyelocytes increased with B50 and B100 compared with diesel (p < 0.05); neutrophils increased with diesel and B50 compared with control (p < 0.05); and macrophages increased with diesel (p < 0.01), B50, and B100 (p < 0.05) compared with control. Biodiesel was more toxic than diesel because it promoted cardiovascular alterations as well as pulmonary and systemic inflammation.

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