Cellular Uptake, Organelle Enrichment, and In Vitro Antioxidation of Fullerene Derivatives, Mediated by Surface Charge.
Haijun MaXiaoyan ZhangYang YangShumu LiJiawei HuoYang LiuMirong GuanMingming ZhenChunying ShuJie LiChun-Ru WangPublished in: Langmuir : the ACS journal of surfaces and colloids (2021)
Hydrophilic fullerene derivatives get notable performance in various biological applications, especially in cancer therapy and antioxidation. The biological behaviors of functional fullerenes are much dependent on their surface physicochemical properties. The excellent reactive oxygen species-scavenging capabilities of functional fullerenes promote their outstanding performances in inhibiting pathological symptoms associated with oxidative stress, including neurodegenerative diseases, cardiovascular diseases, acute and chronic kidney disease, and diabetes. Herein, fullerene derivatives with reversed surface charges in aqueous solutions are prepared: cationic C60-EDA and anionic C60-(EDA-EA). Under the driving force of membrane potential (negative inside) in the cell and mitochondria, C60-EDA is much rapidly taken in by cells and transported into mitochondria compared with C60-(EDA-EA) that is enriched in lysosomes. With high cellular uptake and mitochondrial enrichment, C60-EDA exhibits stronger antioxidation capabilities in vitro than C60-(EDA-EA), indicating its better performance in the therapy of oxidation-induced diseases. It is revealed that the cellular uptake rate, subcellular location, and intracellular antioxidation behavior of fullerene derivatives are primarily mediated by their surface charges, providing new strategies for the design of fullerene drugs and their biological applications.
Keyphrases
- reactive oxygen species
- solar cells
- oxidative stress
- chronic kidney disease
- cardiovascular disease
- cancer therapy
- induced apoptosis
- single cell
- type diabetes
- cell death
- structure activity relationship
- diabetic rats
- drug induced
- drug delivery
- end stage renal disease
- liver failure
- dna damage
- glycemic control
- stem cells
- endothelial cells
- high resolution
- metabolic syndrome
- hepatitis b virus
- respiratory failure
- stress induced
- ischemia reperfusion injury
- cell cycle arrest
- pi k akt