ArticleIranian journal of pharmaceutical research : IJPR
The Protective Effects of Mitochondrial Therapy Against Vincristine- Induced Nephrotoxicity in the Rat's Renal Proximal Tubular Cells.
Article in Iranian journal of pharmaceutical research : IJPR. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Antitumor natural products targeting mitochondrial NADH: ubiquinone oxidoreductase (complex I): a review.Frontiers in pharmacology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The application of vincristine (VCR) in treating a range of cancers is well-documented, showcasing its considerable effectiveness. Nevertheless, its clinical application is constrained by its impact on healthy tissues and various organ systems. Specifically, it can compromise kidney function, resulting in toxicological concerns. Studies have demonstrated that vincristine contributes to nephrotoxicity via the induction of oxidative stress. Objectives: The present research focused on assessing the influence of mitochondrial transplantation in mitigating the mitochondrial and cellular toxicity associated with VCR in renal proximal tubular cells (RPTCs). Methods: This investigation evaluated specific toxicity metrics, including cell death, reactive oxygen species (ROS) generation, decreased mitochondrial membrane potential (MMP), glutathione (GSH) concentration, succinate dehydrogenase (SDH) activity, lipid peroxidation (LPO), and adenosine triphosphate (ATP) levels. Freshly prepared active mitochondria were obtained from the kidneys of Wistar rats. Results: The data demonstrated the cytotoxic effects of VCR on RPTCs. It was further observed that vincristine triggered oxidative stress, characterized by heightened ROS levels, diminished GSH content, decreased SDH activity, and increased lipid peroxidation. Furthermore, VCR caused notable damage to both mitochondrial and lysosomal membranes, along with a significant decrease in ATP content. The innovative strategy of mitochondrial transplantation mitigated oxidative stress, alleviated mitochondrial membrane damage, and prevented ROS-mediated apoptosis signaling induced by vincristine in RPTCs. Our results also indicated an increase in ATP levels within these cells. Conclusions: Our investigation suggests that the proposed treatment modality may prove beneficial in addressing drug-induced nephrotoxicity.
Indexed as
Identifiers
What OpenQuestion holds
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.