Dithiothreitol supplementation mitigates hepatic and renal injury in bile duct ligated mice: Potential application in the treatment of cholestasis-associated complications.
TL;DR: It was found that DTT supplementation alleviated markers of oxidative stress in the liver and kidney of cholestatic animals and histopathological changes and collagen deposition were markedly attenuated by DTT treatment.
About: This article is published in Biomedicine & Pharmacotherapy.The article was published on 2018-01-05. It has received 48 citations till now. The article focuses on the topics: Cholestasis & Oxidative stress.
Citations
More filters
TL;DR: It was found that carnosine and HIS supplementation blunted the Pb-induced oxidative stress and mitochondrial dysfunction in the rat reproductive system, and antioxidative and mitochondria-protective properties serve as primary mechanisms for CAR and HIS against P b-induced reproductive toxicity.
Abstract: Lead (Pb)-induced reproductive toxicity is a well-characterized adverse effect associated with this heavy metal. It has been found that Pb exposure is associated with altered spermatogenesis, increased testicular degeneration, and pathological sperm alterations. On the other hand, it has been reported that Pb-induced reproductive toxicity is associated with increased reactive oxygen species (ROS) formation and diminished antioxidant capacity in the reproductive system. Hence, administration of antioxidants as protective agents might be of value against Pb-induced reproductive toxicity. This study was designed to investigate whether carnosine (CAR) and histidine (HIS) supplementation would mitigate the Pb-induced reproductive toxicity in male rats. Animals received Pb (20 mg/kg/day, oral, 14 consecutive days) alone or in combination with CAR (250 and 500 mg/kg/day, oral, 14 consecutive days) or HIS (250 and 500 mg/kg/day, oral, 14 consecutive days). Pb toxicity was evident in the reproductive system by a significant increase in tissue markers of oxidative stress along with severe histopathological changes, seminal tubule damage, tubular desquamation, low spermatogenesis index, poor sperm parameters, and impaired sperm mitochondrial function. It was found that CAR and HIS supplementation blunted the Pb-induced oxidative stress and mitochondrial dysfunction in the rat reproductive system. Thereby, antioxidative and mitochondria-protective properties serve as primary mechanisms for CAR and HIS against Pb-induced reproductive toxicity.
80 citations
Cites methods from "Dithiothreitol supplementation miti..."
...Afterward, the DCF fluorescence intensity was recorded using a FLUOstar Omega®multifunctional microplate reader (BMG LABTECH, Germany) (λ excitation = 485 nm and λ emission = 525 nm) [52, 58]....
[...]
TL;DR: Evaluated pathologic effects of cholestasis-associated reproductive toxicity in male and female rats is restrictedly coupled with severe oxidative stress and mitochondrial impairment.
48 citations
TL;DR: Mitochondrial dysfunction and energy metabolism disturbances are introduced as a fundamental mechanism involved in the pathogenesis of bile acids-associated renal injury during cholestasis.
45 citations
TL;DR: The current review focuses on the footprints of mitochondrial impairment in the etiology of xenobiotics-induced Fanconi's Syndrome and the importance of mitochondria protecting agents and their preventive/therapeutic capability against FS is highlighted.
35 citations
TL;DR: It was found that NAC treatment significantly mitigated biomarkers of oxidative stress and alleviated tissue histopathological changes in cirrhotic rats, representing NAC as a potential protective agent with therapeutic capability in cholestasis and its associated complications.
Abstract: Cholestasis is a multifaceted clinical complication. Obstructive jaundice induced by bile duct ligation (BDL) is known as an animal model to investigate cholestasis and its associated complications...
30 citations
Cites background from "Dithiothreitol supplementation miti..."
...…for 28 consecutive days in BDL rats) could serve as a protective option against cholestasisinduced organ injury (Assimakopoulos et al., 2007; Heidari, Ghanbarinejad, Mohammadi, et al., 2018b; Heidari et al., 2017; Heidari et al., 2018; Heidari, Niknahad, et al., 2018; Jamshidzadeh et al., 2017b)....
[...]
References
More filters
TL;DR: This research presents a meta-analysis of Anatomia e Istologia Patologica, a large quantity of which has never before been published in a peer-reviewed journal, which aims to provide real-time information about the immune system’s response to disease.
4,655 citations
TL;DR: The role of mitochondrial glutathione in cellular response to toxic exposures that include loss of the homeostases of Ca2+ and protein thiols is described.
Abstract: Glutathione as reduced glutathione (GSH) and as the disulfide (GSSG) is a unique peptide that continues to interest toxicologists-as reflected in the numerous symposia and reviews ( 1-6). This article undertakes to describe the role of mitochondrial glutathione in cellular response to toxic exposures that include loss of the homeostases of Ca2+ and protein thiols. Because of the numerous reviews on the glutathione S-transferases (7-10), only the per oxidase activity of membrane-associated glutathione S-transferases is dis cussed. Mammalian cells have evolved protective mechanisms to minimize in jurious events that result from toxic chemicals and normal oxidative products of cellular metabolism. A major endogenous protective system is the glu tathione redox cycle (2). Glutathione is present in high concentrations as GSH in most mammalian cells (generally in the millimolar range), with minor fractions being GSSG, mixed disulfides of GSH and other cellular thiols, and minor amounts of thioethers ( 1) . GSH acts both as a nucleophilic "scavenger" of numerous compounds and their metabolites, via enzymatic and chemical mechanisms, converting electrophilic centers to thioether bonds, and as a substrate in the GSH peroxidase-mediated destruction of hydroperoxides. GSH depletion to about 20-30% of total glutathione levels can impair the cell's defense against the toxic actions of such compounds and may lead to cell injury and death (3, 1 1) .
754 citations
TL;DR: This review will highlight major concepts and recent insights related to the role of nitric oxide and reactive nitrogen oxide intermediates in chronic liver injury, with special reference to NO interactions with ROI and potential anti-brogenic action of NO, and indicate reactive oxygen intermediates (ROI, i.e. a major feature of hepatic oxidative stress).
712 citations
TL;DR: Simple grading and staging systems for chronic hepatitis, including the IASL, Batts-Ludwig, and Metavir systems, are most appropriate for management of individual patients, while more complex systems such as the Histology Activity Index (HAI) are appropriate for evaluation of large cohorts of patients when statistical analysis is required.
683 citations
TL;DR: Reactive oxidant species likely contribute to both onset and progression of fibrosis as induced by alcohol, viruses, iron or copper overload, cholestasis, hepatic blood congestion and many if not all chronic disease processes affecting hepatic tissue.
606 citations