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Polydopamine nanoparticles as a potential non-pharmaceutical antioxidant tool against mitochondrial disorders

ABSTRACT: Mitochondrial disorders are a subset of hereditary diseases characterized by defects in mitochondrial functionality due to mutations in genes in nuclear or mitochondrial DNA. The molecular hallmarks of mitochondrial disorders include a high production of reactive oxygen species (ROS), morphological and functional mitochondrial aberrations, and metabolic impairments. From a systemic perspective, these molecular and cellular impairments can lead to severe disorders affecting the central nervous system, besides to muscles, heart, and gastrointestinal problems. The treatment of mitochondrial diseases with antioxidant moieties like idebenone and resveratrol has been proposed and tested as a potential therapy for these disorders. Polydopamine nanoparticles (PDNPs) are nanostructures derived from the oxidative self-polymerization of dopamine and characterized by high biocompatibility and biodegradability, the ability to be easily functionalized with active molecules, high antioxidant properties, and the ability to act as photothermal conversion agents when irradiated with near infrared (NIR) light. In this work we tested the potential of PDNPs as a non-pharmaceutical treatment for two mitochondrial diseases, namely mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) and progressive external ophthalmoplegia (PEO). We tested PDNPs on fibroblasts derived from healthy subjects and fibroblasts derived from MELAS and PEO patients. The cells were first characterized from a molecular point of view through proteomic analysis. Then, the biocompatibility, internalization rate, intracellular localization, and protective antioxidant properties of PDNPs were assessed. Lastly, the antioxidant properties of PDNPs were also confirmed on an in vivo model based on zebrafish embryos. Our data demonstrates the ability of PDNPs to protect both healthy and patient-derived cells from ROS-induced damage, thus preventing the increment of oxidative stress, ROS-induced apoptosis, and mitochondrial dysfunctions. Eventually, PDNPs showed the capacity to protect zebrafish embryos from pro-oxidative stimuli. Altogether, this work demonstrates the potential of polydopamine nanostructures as an effective countermeasure for some of the molecular hallmarks associated with mitochondrial disorders, paving the way for the future exploitation in clinical applications.

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ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Fibroblast

SUBMITTER: Martina Bartolucci

LAB HEAD: Andrea Petretto

PROVIDER: PXD063824 | Pride | 2026-07-16

REPOSITORIES: Pride

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Project description:Reactive oxygen species (ROS) are active molecules involved in several biological functions. When the production of ROS is not counterbalanced by the action of protective antioxidant mechanisms present in living organisms, a condition of oxidative stress can arise with consequent damage to biological structures. The brain is one of the main ROS-generating organs in the human body, with the consequence that most neurological disorders are associated with the overproduction of ROS. Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is a neurodegenerative disease associated with mutations in the sacsin gene (SACS). At a cellular level, ARSACS is characterized by mitochondrial impairments, a reduction of bioenergetic processes, and by both an over-production of and an over sensitivity to ROS. Several antioxidant molecules have been proposed as a potential treatment for ARSACS, such as idebenone and resveratrol. Polydopamine nanoparticles (PDNPs) gained significant attention in recent years owing to their peculiar physic-chemical properties, and especially because of their antioxidant activity. PDNPs have shown a great ROS scavenging capacity that, combined with their completely organic nature that grants them the ability to be degraded and excreted by living organisms, make them a promising candidate in the treatment of oxidative stress-related disorders. In this work we assessed the effect of PDNPs upon human fibroblasts; in particular, we investigated the effects of PDNPs on populations of fibroblasts derived from healthy subjects and of fibroblasts derived from ARSACS patients, in terms of antioxidant properties and protein expression. PDNPs interaction with fibroblasts was analyzed in terms of biocompatibility, internalization and uptake pathway, reduction of ROS levels, prevention of ROS-induced apoptosis/necrosis, and protective action upon ROS-induced mitochondrial dysfunctions. Moreover, a complete proteomic analysis of the cells was performed to assess differences in terms of protein expression upon different treatments. Altogether, our data showed that PDNPs can partially counteract ROS-induced damages in both healthy and ARSACS patients-derived fibroblasts, making them a potential therapeutic candidate to treat or at least ameliorate the condition of oxidative stress associated with ARSACS disease.

			Action	DRS
	MELAS_CTRL_1_42.raw	Raw
	MELAS_CTRL_2_43.raw	Raw
	MELAS_CTRL_3_44.raw	Raw
	MELAS_CTRL_4_45.raw	Raw
	MELAS_CTRL_5_46.raw	Raw

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Polydopamine nanoparticles as a potential non-pharmaceutical antioxidant tool against mitochondrial disorders

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