ArticleEnvironmental science and pollution research international2020
Multi-walled carbon nanotubes induce oxidative stress, apoptosis, and dysfunction in isolated rat heart mitochondria: protective effect of naringin.
Article in Environmental science and pollution research international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 22 citations in OpenAlex.
- Naringin and hesperidin protect ovarian granulosa cells from cisplatin-induced mitochondrial dysfunction by enhancing bioenergetics and mitophagy.Biology direct · 2026Article
- Naringin regulates the cGAS-STING pathway to improve mitochondrial dysfunction and ferroptosis after myocardial ischemia-reperfusion injury.Cytotechnology · 2025Article
- Assessment of Pristine Carbon Nanotubes Toxicity in Rodent Models.International journal of molecular sciences · 2022Review
- Do Carbon Nanotubes and Asbestos Fibers Exhibit Common Toxicity Mechanisms?Nanomaterials (Basel, Switzerland) · 2022Review
- Therapeutic Approach of Flavonoid in Ameliorating Diabetic Cardiomyopathy by Targeting Mitochondrial-Induced Oxidative Stress.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Multi-walled carbon nanotubes (MWCNTs) are material with exclusive features that can be applied in different fields including industrial and medicine. It has been determined that the accumulation of MWCNTs in the organs is along with genotoxic and cytotoxic injuries. Previous studies have shown mitochondrial dysfunction in MWCNTs exposure with cell lines, but their exact mechanisms with isolated mitochondria have remained unclear. The present study evaluated toxicity induced by MWCNTs in isolated rat heart mitochondria and protective effect of naringin. Our results showed that MWCNTs toxicity caused the prevention of heart mitochondrial complex II activity. Treatment of isolated heart mitochondria with MWCNTs led to an increase in mitochondrial reactive oxygen species (ROS) generation, mitochondrial membrane potential (MMP) collapse, and mitochondrial malondialdehyde (MDA) and a decrease in mitochondrial glutathione (GSH) level and mitochondrial catalase (CAT) activity. Pretreatment of isolated heart mitochondria with naringin decreased mitochondrial oxidative damage through decreasing lipid peroxidation, returned mitochondrial complex II changes, decreasing MMP collapse and ROS production, and restoration of GSH level and CAT activity. Our findings indicated that MWCNTs had toxic effects on isolated heart mitochondria by inducing oxidative stress and possibly apoptosis pathway. The protection effects of naringin may be accompanied by mitochondrial conservation by its antioxidant property or due to its free radical scavenging. Our findings indicated that naringin had a possible role in preventing the mitochondria complaints in the heart.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.