The mechanisms of arsenic-induced ovotoxicity, ultrastructural alterations, and autophagic related paths: An enduring developmental study in folliculogenesis of mice

Ommati, Mohammad Mehdi; Shi, Xinjian; Li, Huifeng; Zamiri, Mohammad Javad; Farshad, Omid; Jamshidzadeh, Akram; Heidari, Reza; Ghaffari, Hasti; Zaker, Ladan; Sabouri, Samira; Chen, Yuanyu

doi:10.1016/j.ecoenv.2020.110973

Cited by 60 publications

(26 citation statements)

References 69 publications

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“…The capacity of isolated mitochondria to capture the rhodamine 123 was used to estimate mitochondrial depolarization. [ 21,37–39 ] Briefly, 1 ml of the mitochondria‐rich fractions (1 mg protein/ml in the depolarization assay buffer) were incubated with rhodamine 123 (final concentration of 10 µM, 15 min in the dark with continuous shaking). Afterward, the samples were centrifuged (15,000 g , 5 min, 4°C) and the fluorescence intensity of the supernatant was assessed (Germany, λ excitation = 485 nm and λ emission = 525 nm; FLUOstar Omega® fluorimeter).…”

Section: Methodsmentioning

confidence: 99%

“…The capacity of isolated mitochondria to capture the rhodamine 123 was used to estimate mitochondrial depolarization. [21,[37][38][39] Briefly, 1 ml of the mitochondria-rich fractions (1 mg protein/ml in the depolarization assay buffer) were incubated with rhodamine 123 (final concentration of 10 µM, 15 min in the dark with continuous shaking).…”

Section: Mitochondrial Depolarizationmentioning

confidence: 99%

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Disturbed mitochondrial redox state and tissue energy charge in cholestasis

Ghanbarinejad

Ommati

Jia

et al. 2021

J Biochem & Molecular Tox

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The liver is the primary organ affected by cholestasis. However, the brain, skeletal muscle, heart, and kidney are also severely influenced by cholestasis/cirrhosis. However, little is known about the molecular mechanisms of organ injury in cholestasis. The current study was designed to evaluate the mitochondrial glutathione redox state as a significant index in cell death. Moreover, tissue energy charge (EC) was calculated. Rats underwent bile duct ligation (BDL) and the brain, heart, liver, kidney, and skeletal muscle mitochondria were assessed at scheduled time intervals (3, 7, 14, and 28 days after BDL). A significant decrease in mitochondrial glutathione redox state and EC was detected in BDL animals. Moreover, disturbed mitochondrial indices were evident in different organs of BDL rats. These data could offer new insight into the mechanisms of organ injury and the source of oxidative stress during cholestasis and might provide novel therapeutic strategies against these complications.

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Section: Methodsmentioning

confidence: 99%

Section: Mitochondrial Depolarizationmentioning

confidence: 99%

Disturbed mitochondrial redox state and tissue energy charge in cholestasis

Ghanbarinejad

Ommati

Jia

et al. 2021

J Biochem & Molecular Tox

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“…Reactive oxygen species formation in the kidney was estimated based on a previously described procedure [54][55][56]. Briefly, 200 mg of the kidney tissue was homogenized in 5 ml of ice-cooled Tris-HCl buffer (40 mM, pH = 7.4).…”

Section: Reactive Oxygen Species Formationmentioning

confidence: 99%

Taurine mitigates bile duct obstruction-associated cholemic nephropathy: effect on oxidative stress and mitochondrial parameters

Abdoli¹,

Sadeghian²,

Azarpira³

et al. 2021

ceh

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Aim of the study: Cholestasis is a serious complication affecting other organs such as the liver and kidney. Oxidative stress and mitochondrial impairment are proposed as the primary mechanisms for cholestasis-induced organ injury. Taurine (TAU) is the most abundant free amino acid in the human body, which is not incorporated in the structure of proteins. Several pharmacological effects have been attributed to TAU. It has been reported that TAU effectively mitigated oxidative stress and modulated mitochondrial function. The current study aimed to evaluate the impact of TAU on oxidative stress biomarkers and mitochondrial parameters in the kidney of cholestatic animals. Material and methods: Bile duct ligated (BDL) rats were used as an antioxidant model of cholestasis. Animals were treated with TAU (500 and 1000 mg/kg, oral) for seven consecutive days. Animals were anesthetized (thiopental 80 mg/kg, i.p.), and kidney and blood specimens were collected. Results: Severe elevation in serum and urine biomarkers of renal injury was evident in the BDL group. Significant lipid peroxidation, reactive oxygen species (ROS) formation, and protein carbonylation were detected in the kidney of BDL animals. Furthermore, depleted glutathione reservoirs and a significant decrease in the antioxidant capacity of renal tissue were detected in cholestatic rats. Renal tubular atrophy and interstitial inflammation were evident in BDL animals. Cholestasis also caused significant mitochondrial dysfunction in the kidney. TAU significantly prevented cholestasis-induced renal injury by inhibiting oxidative stress and mitochondrial impairment. Conclusions: These data indicate TAU as a potential therapeutic agent in the management of cholestasis-induced renal injury.

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“…[51] Oxidative stress, mitochondrial injury, and disturbances in cellular calcium ion (Ca 2+ ) homeostasis (ER stress) are mechanistically interrelated events that could finally lead to cell death through apoptosis and/or autophagy. [51][52][53][54] In the following section, the reported mechanisms of hepatotoxicity induced by anti-COVID-19 drugs are reviewed (Table 1).…”

Section: Drug-induced Hepatotoxicity (Dili)mentioning

confidence: 99%

Drug‐induced organ injury in coronavirus disease 2019 pharmacotherapy: Mechanisms and challenges in differential diagnosis and potential protective strategies

Ommati

Mobasheri

Heidari

2021

J Biochem & Molecular Tox

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The world is currently facing an unprecedented pandemic caused by a newly recognized and highly pathogenic coronavirus disease 2019 (COVID‐19; induced by SARS‐CoV‐2 virus), which is a severe and ongoing threat to global public health. Since COVID‐19 was officially declared a pandemic by the World Health Organization in March 2020, several drug regimens have rapidly undergone clinical trials for the management of COVID‐19. However, one of the major issues is drug‐induced organ injury, which is a prominent clinical challenge. Unfortunately, most drugs used against COVID‐19 are associated with adverse effects in different organs, such as the kidney, heart, and liver. These side effects are dangerous and, in some cases, they can be lethal. More importantly, organ injury is also a clinical manifestation of COVID‐19 infection. These adverse reactions are increasingly recognized as outcomes of COVID‐19 infection. Therefore, the differential diagnosis of drug‐induced adverse effects from COVID‐19‐induced organ injury is a clinical complication. This review highlights the importance of drug‐induced organ injury, its known mechanisms, and the potential therapeutic strategies in COVID‐19 pharmacotherapy. We review the potential strategies for the differential diagnosis of drug‐induced organ injury. This information can facilitate the development of therapeutic strategies, not only against COVID‐19 but also for future outbreaks of other emerging infectious diseases.

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The mechanisms of arsenic-induced ovotoxicity, ultrastructural alterations, and autophagic related paths: An enduring developmental study in folliculogenesis of mice

Cited by 60 publications

References 69 publications

Disturbed mitochondrial redox state and tissue energy charge in cholestasis

Disturbed mitochondrial redox state and tissue energy charge in cholestasis

Taurine mitigates bile duct obstruction-associated cholemic nephropathy: effect on oxidative stress and mitochondrial parameters

Drug‐induced organ injury in coronavirus disease 2019 pharmacotherapy: Mechanisms and challenges in differential diagnosis and potential protective strategies

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