Multi-walled carbon nanotubes induce oxidative stress, apoptosis, and dysfunction in isolated rat heart mitochondria: protective effect of naringin

Salehcheh, Maryam; Alboghobeish, Soheila; Dehghani, Mohammad Amin; Zeidooni, Leila

doi:10.1007/s11356-020-07943-w

Cited by 15 publications

(13 citation statements)

References 52 publications

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“…Furthermore, data in our study also suggested that the increased rate of apoptotic and necrotic erythrocytes may have happened because of damages to cell membranes caused by direct contact of these models with CNFs or by increased oxidative stress, which was inferred through different biomarkers (H2O2, ROS and TBARS). However, assumingly, CNFs induced increased expression of apoptosis genes (as demonstrated by Lee et al (2015)], mitochondrial membrane potential collapse (as suggested by Salehcheh et al (2020)], DNA damage [whose plausibility has already been demonstrated by Li et al (2005) and Zhu et al (2007)], and caspase activation [as suggested by Sohaebuddin et al (2010)]. Shen et al (2010) and Wang et al (2012) have reported that CNs can cause, Ca2 + homeostasis imbalance and mitochondrial damage, as well as oxidative stress.…”

Section: Discussionmentioning

confidence: 94%

“…These data are particularly interesting, since they corroborate other studies that have already shown the induction of cell death processes in different model systems exposed to CNFs (either in vitro or in vivo ). This finding is indicative of nanomaterials activating apoptotic and necrotic pathways through different pathways (Bottini et al, 2006; Elgrabli et al, 2008; Ravichandran et al, 2009; Patlolla et al, 2010; Srivastava et al, 2011; Wang et al, 2012; Kim et al, 2014; Salehcheh et al, 2020). Furthermore, data in our study also suggested that the increased rate of apoptotic and necrotic erythrocytes may have happened because of damages to cell membranes caused by direct contact of these models with CNFs or by increased oxidative stress, which was inferred through different biomarkers (H2O2, ROS and TBARS).…”

Section: Discussionmentioning

confidence: 95%

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Can Carbon Nanofibers Affect Anurofauna? Study Involving NeotropicalPhysalaemus cuvieri(Fitzinger, 1826) Tadpoles

Guimarães

Estrela

Rodrigues

et al. 2021

Preprint

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Although carbon nanotubes (CNTs) toxicity in different experimental systems (in vivo and in vitro) is known, little is known about the toxic effects of carbon nanofibers (CNFs) on aquatic vertebrates. We herein investigated the potential impact of CNFs (1 and 10 mg/L) by using Physalaemus cuvieri tadpoles as experimental model. CNFs were able to induce nutritional deficit in animals after 48-h exposure to them, and this finding was inferred by reductions observed in body concentrations of total soluble carbohydrates, total proteins, and triglycerides. The increased production of hydrogen peroxide, reactive oxygen species and thiobarbituric acid reactive substances in tadpoles exposed to CNFs has suggested REDOX homeostasis change into oxidative stress. This process was correlated to the largest number of apoptotic and necrotic cells in the blood of these animals. On the other hand, the increased superoxide dismutase and catalase activity has suggested that the antioxidant system of animals exposed to CNFs was not enough to maintain REDOX balance. In addition, CNFs induced increase in acetylcholinesterase and butyrylcholinesterase activity, as well as changes in the number of neuromats evaluated on body surface (which is indicative of the neurotoxic effect of nanomaterials on the assessed model system). To the best of our knowledge, this is the first report on the impact of CNFs on amphibians; therefore, it broadened our understanding about ecotoxicological risks associated with their dispersion in freshwater ecosystems and possible contribution to the decline in the populations of anurofauna species.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 95%

Can Carbon Nanofibers Affect Anurofauna? Study Involving NeotropicalPhysalaemus cuvieri(Fitzinger, 1826) Tadpoles

Guimarães

Estrela

Rodrigues

et al. 2021

Preprint

View full text Add to dashboard Cite

show abstract

“…AP-1 and NF-ĸB (redox-sensitive transcription factors), which are activated by asbestos/CNT exposure, regulate expression of several genes involved in inflammation, proliferation, apoptosis and the carcinogenesis process. Several studies report the mitochondria-mediated production of ROS, their localization and the resulting damage in response to asbestos/CNT exposures [ 70 , 71 , 72 , 73 , 74 , 75 , 76 , 77 , 78 ].…”

Section: Do Asbestos and Cnts Have The Same Mechanism Of Pathogenicity?mentioning

confidence: 99%

Do Carbon Nanotubes and Asbestos Fibers Exhibit Common Toxicity Mechanisms?

et al. 2022

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During the last two decades several nanoscale materials were engineered for industrial and medical applications. Among them carbon nanotubes (CNTs) are the most exploited nanomaterials with global production of around 1000 tons/year. Besides several commercial benefits of CNTs, the fiber-like structures and their bio-persistency in lung tissues raise serious concerns about the possible adverse human health effects resembling those of asbestos fibers. In this review, we present a comparative analysis between CNTs and asbestos fibers using the following four parameters: (1) fibrous needle-like shape, (2) bio-persistent nature, (3) high surface to volume ratio and (4) capacity to adsorb toxicants/pollutants on the surface. We also compare mechanisms underlying the toxicity caused by certain diameters and lengths of CNTs and asbestos fibers using downstream pathways associated with altered gene expression data from both asbestos and CNT exposure. Our results suggest that indeed certain types of CNTs are emulating asbestos fiber as far as associated toxicity is concerned.

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“…However, in other cardiac models, flavanone has been demonstrated to modulate mitochondrial function in cardiomyocytes. Previously, flavanone was found to ameliorate mitochondrial disruption in cardiomyocytes by reducing impaired mitochondrial membrane potential and suppressing mitochondrial ROS levels and increase mitochondrial antioxidant via regulation of AMPK-mTOR signaling pathways [ 130 , 131 ]. Moreover, flavanone was able to alleviate mitochondrial membrane potential collapse and preserve mitochondrial complex II activity on isolated heart mitochondria [ 131 ].…”

Section: Therapeutic Role Of Flavonoid In Alleviating Mitochondrial Dysfunction-induced Oxidative Stress In Diabetic Cardiomyopathymentioning

confidence: 99%

“…Previously, flavanone was found to ameliorate mitochondrial disruption in cardiomyocytes by reducing impaired mitochondrial membrane potential and suppressing mitochondrial ROS levels and increase mitochondrial antioxidant via regulation of AMPK-mTOR signaling pathways [ 130 , 131 ]. Moreover, flavanone was able to alleviate mitochondrial membrane potential collapse and preserve mitochondrial complex II activity on isolated heart mitochondria [ 131 ]. Aside from that, Ca 2+ overload was reduced significantly with the treatment of flavanone and hence reviving mitochondrial function in the heart [ 132 ].…”

Section: Therapeutic Role Of Flavonoid In Alleviating Mitochondrial Dysfunction-induced Oxidative Stress In Diabetic Cardiomyopathymentioning

confidence: 99%

Therapeutic Approach of Flavonoid in Ameliorating Diabetic Cardiomyopathy by Targeting Mitochondrial-Induced Oxidative Stress

Sapian

Taib

Latip

et al. 2021

IJMS

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Diabetes cardiomyopathy is one of the key factors of mortality among diabetic patients around the globe. One of the prior contributors to the progression of diabetic cardiomyopathy is cardiac mitochondrial dysfunction. The cardiac mitochondrial dysfunction can induce oxidative stress in cardiomyocytes and was found to be the cause of majority of the heart morphological and dynamical changes in diabetic cardiomyopathy. To slow down the occurrence of diabetic cardiomyopathy, it is crucial to discover therapeutic agents that target mitochondrial-induced oxidative stress. Flavonoid is a plentiful phytochemical in plants that shows a wide range of biological actions against human diseases. Flavonoids have been extensively documented for their ability to protect the heart from diabetic cardiomyopathy. Flavonoids’ ability to alleviate diabetic cardiomyopathy is primarily attributed to their antioxidant properties. In this review, we present the mechanisms involved in flavonoid therapies in ameliorating mitochondrial-induced oxidative stress in diabetic cardiomyopathy.

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Multi-walled carbon nanotubes induce oxidative stress, apoptosis, and dysfunction in isolated rat heart mitochondria: protective effect of naringin

Cited by 15 publications

References 52 publications

Can Carbon Nanofibers Affect Anurofauna? Study Involving NeotropicalPhysalaemus cuvieri(Fitzinger, 1826) Tadpoles

Can Carbon Nanofibers Affect Anurofauna? Study Involving NeotropicalPhysalaemus cuvieri(Fitzinger, 1826) Tadpoles

Do Carbon Nanotubes and Asbestos Fibers Exhibit Common Toxicity Mechanisms?

Therapeutic Approach of Flavonoid in Ameliorating Diabetic Cardiomyopathy by Targeting Mitochondrial-Induced Oxidative Stress

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