Vanadium compounds induced mitochondria permeability transition pore (PTP) opening related to oxidative stress

Zhao, Yuebin; Ye, Lihua; Liu, Huixue; Xia, Qing; Zhang, Yue; Yang, Xiaoda; Wang, Kui

doi:10.1016/j.jinorgbio.2009.11.007

Cited by 176 publications

(106 citation statements)

References 52 publications

(71 reference statements)

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“…Opening of the MPTP causes mitochondrial swelling and the change in mitochondrial volume due to colloidal osmotic effects of solute flux into and out of the mitochondrial matrix was measured by monitoring the absorbance at 520 nm (A 520 ) as described (Zhao et al, 2010). Briefly, isolated mitochondria (approximately 500 mg) in 1 ml of respiration buffer were pre-incubated at 30 1C for 10 min.…”

Section: Mitochondrial Swelling Assaysmentioning

confidence: 99%

Vasopressin attenuates ischemia–reperfusion injury via reduction of oxidative stress and inhibition of mitochondrial permeability transition pore opening in rat hearts

Nazari

Sadr

Faghihi

et al. 2015

European Journal of Pharmacology

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Section: Mitochondrial Swelling Assaysmentioning

confidence: 99%

Vasopressin attenuates ischemia–reperfusion injury via reduction of oxidative stress and inhibition of mitochondrial permeability transition pore opening in rat hearts

Nazari

Sadr

Faghihi

et al. 2015

European Journal of Pharmacology

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“…18,48 This is similar to the vanadium-induced toxicity on cellular mitochondria. 46,49 As discussed earlier, the exposure of bacteria to V metal, V 2 O 3 , VO 2 , and V 2 O 5 nanofilms may elevate intracellular ROS levels and thus cause oxidative stress and damage. To verify this, we further used DCFH-DA fluorescence dye to visualize intracellular ROS levels, which can be indicated by green fluorescence.…”

mentioning

confidence: 94%

A functionalized surface modification with vanadium nanoparticles of various valences against implant-associated bloodstream infection

Wang¹,

Zhou²,

Guo³

et al. 2017

IJN

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Bloodstream infection, especially with implants involved, is an often life-threatening condition with high mortality rates, imposing a heavy burden on patients and medical systems. Herein, we firstly deposited homogeneous vanadium metal, V 2 O 3 , VO 2 , and V 2 O 5 nanofilms on quartz glass by magnetron sputtering. Using these platforms, we further investigated the potential antimicrobial efficiency of these nano-VO x films and the interactions of human erythrocytes and bacteria (methicillin-resistant Staphylococcus aureus and Pseudomonas aeruginosa ) with our samples in a novel cell–bacteria coculture model. It was demonstrated that these nano-VO x precipitated favorable antibacterial activity on both bacteria, especially on S. aureus , and this effect increased with higher vanadium valence. A possible mechanism accountable for these results might be elevated levels of vanadium-induced intracellular reactive oxygen species. More importantly, based on hemolysis assays, our nano-VO x films were found to be able to kill prokaryotic cells but were not toxic to mammalian cells, holding the potential for the prevention of implant-related hematogenous infections. As far as we know, this is the first report wherein such nano-VO x films have assisted human erythrocytes to combat bacteria in a valence-dependent manner. Additionally, vanadium ions were released from these nano-VO x films in a sustained manner, and low-valence films possessed better biocompatibility with human fibroblasts. This work may provide new insights for biomedical applications of inorganic vanadium compounds and attract growing attention in this field. From the perspective of surface modification and functionalization, this study holds promise to avail the prophylaxis of bloodstream infections involving implantable biomedical devices.

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“…The mitochondria, as the main cellular source for ROS production, are an important target for vanadium accumulation (Soares et al, 2007). The mechanism by which vanadium compounds promote mitochondrial ROS generation may be due to impaired activity of antioxidant enzymes and/or impaired respiration from vanadium interacting with mitochondrial's inner membrane (Zhao et al, 2010). Also, increased LPO and MDA by vanadium exposure could be explained by vanadium's ability to generate hydroxyl radicals via Fenton-like reaction (Shi et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Effects of vanadium on oxidative stress and electrolytes balance of dyslipidemic male rats treated with simvastatin

Eweda¹,

Rezk²,

Ahmed³

et al. 2018

Afr. J. Pharm. Pharmacol.

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Dyslipidaemia is characterised by enhanced production of reactive oxygen species and increased oxidative stress, which may affect liver, kidney and heart function. It is considered as a critical risk factor for cardiovascular and liver diseases. The aim of our study was to assess the effect of vanadium chloride on the oxidative stress state of liver, kidney and heart functions along with electrolyte balance during treatment of dyslipidemia using simvastatin in an animal model. Rats were assigned to 1 of 5 groups: group 1, control group; group 2, received high fat diet (HFD); group 3, received HFD and 30 mg/kg body weight (BW) simvastatin; group 4, received HFD and 15 mg/kg BW vanadium chloride and group 5, received HFD, simvastatin and vanadium chloride. Drugs were administered orally by gavage for the last week of the experimental period. HFD was found to elicit a significant decrease (P ≤ 0.05) in non-protein sulfhydryls and significant increases (P ≤ 0.05) in hepatic and cardiac malondialdehyde (MDA), serum creatine kinase, lactate dehydrogenase, creatinine, urea, uric acid, calcium, sodium and potassium. Oral administration of vanadium chloride did not synergize simvastatin to ameliorate the negative effects of HFD, instead it worsens the negative effect of the HFD. Vanadium chloride administration decreased the concentration of non-protein sulfhydryls and increased MDA concentration in liver and heart tissues. It also caused further increase in the serum concentration of all measured serum parameters. These data proved that the vanadium concentration used in this study is not safe or efficient in ameliorating the oxidative stress or in improving kidney or heart functions in dyslipidemic rats.

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Vanadium compounds induced mitochondria permeability transition pore (PTP) opening related to oxidative stress

Cited by 176 publications

References 52 publications

Vasopressin attenuates ischemia–reperfusion injury via reduction of oxidative stress and inhibition of mitochondrial permeability transition pore opening in rat hearts

Vasopressin attenuates ischemia–reperfusion injury via reduction of oxidative stress and inhibition of mitochondrial permeability transition pore opening in rat hearts

A functionalized surface modification with vanadium nanoparticles of various valences against implant-associated bloodstream infection

Effects of vanadium on oxidative stress and electrolytes balance of dyslipidemic male rats treated with simvastatin

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