The biological effects of drug vehicles are often overlooked, often leading to artifacts in acetaminophen-induced liver injury assessment. Therefore, we decided to investigate the effect of dimethylsulfoxide, dimethylformamide, propylene glycol, ethanol, and Tween 20 on acetaminophen-induced liver injury. C57BL/6 male mice received a particular drug vehicle (0.6 or 0.2 mL/kg, i.p.) 30 min before acetaminophen administration (300 mg/kg, i.p.). Control mice received vehicle alone. Liver injury was assessed by measuring the concentration of alanine aminotransferase in plasma and observing histopathological changes. The level of reduced glutathione (GSH) was assessed by measuring total nonprotein hepatic sulfhydrils. Dimethylsulfoxide and dimethylformamide (at both doses) almost completely abolished acetaminophen toxicity. The higher dose of propylene glycol (0.6 mL/kg) was markedly protective, but the lower dose (0.2 mL/kg) was only slightly protective. These solvents also reduced acetaminophen-induced GSH depletion. Dimethylformamide was protective when given 2 h before or 1 h after acetaminophen administration, but was ineffective if given 2.5 h after acetaminophen. Ethanol at the higher dose (0.6 mL/kg) was partially protective, whereas ethanol at the lower dose (0.2 mL/kg) as well as Tween 20 at any dose had no influence. None of the vehicles (0.6 mL/kg) was hepatotoxic per se, and none of them was protective in a model of liver injury caused by D-galactosamine and lipopolysaccharide.
Nonetheless, CBS remains commonly underreported, under recognized and/or misrecognized. Albeit the treatment recommendations and guidelines are not yet fully established, it is important to raise awareness of this specific and distinct condition, which inevitably implicates many differential diagnostic deliberations.
Background: Schizophrenia is a multifactorial neurodevelopmental disorder associated with cognitive dysfunction and changes in primary sensory processing. This article aims to explore the current insights into the relationship between schizophrenia and different visual disturbances.Methods: To provide a literature review of visual impairments in schizophrenia, we performed a PubMed/MEDLINE and Scopus search to identify all articles in English on the topic up to the end of 2018.Results: Multiple retinal functional and structural abnormalities are found in patients with schizophrenia. Wider retinal venules suggest chronically insufficient brain supply of oxygen and this could contribute to the occurrence of psychotic symptoms. Optical coherence tomography studies showed that retinal nerve fiber layer, macular thickness, and macular volume were significantly lowered in the chronic phase of schizophrenia. Results from electroretinogram recordings have demonstrated different declinations such as abnormalities of a -wave activity in the photoreceptors or b -wave activity in the bipolar and Muller cells. Abnormalities in eye movements, such as a notable decrease in saccades and smooth pursuit eye movements, are one of the most reliable and reproducible impairments associated with schizophrenia. Disrupted visual processing of the magnocellular pathway may result in a decrease of contrast sensitivity, sensory processing, orientation discrimination, visual integration, trajectory and spatial localization, backward masking and motion tracking. Visual perceptual abnormalities occur in more than 60% of schizophrenic patients and these are visual hallucinations, perceptual distortion of colors, shapes and light intensity, decrease in contour integration and surround suppression. Other, frequently present eye disorders include impaired visual acuity, strabismus and nystagmus.Conclusion: Visual impairments are one of the most important features of schizophrenia, which could help in defining the disease state and assigning appropriate treatment.
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