Goncalo Teixeira 2018 MiPschool Tromso C1

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Subchronic in vivo study for the evaluation of hepatic mitochondrial toxicity induced by silver nanoparticles.

Link: MitoEAGLE

Goncalo Teixeira da Silva R, Teodoro JS, Rolo AP, Palmeira CM (2018)

Event: MiPschool Tromso-Bergen 2018

COST Action MitoEAGLE

Manufactured nanomaterials have been of extreme importance due to the beneficial physicochemical properties they possess compared to bulk parental materials. However, the properties that make them so attractive are also the same that can cause harm both to humans and environment. Among all used nanoparticles, silver nanoparticles (AgNPs) have the highest level of commercialization. The main toxicological concern is the fact that AgNPs preferentially accumulate in mitochondria. Since mitochondria have an essential bioenergetic function, impairment of mitochondria by nanoparticles may have drastic consequences on cellular function.

Sprague–Dawley rats were weekly intraperitoneally injected with either 10- or 75-nm AgNPs, with or without a previous injection of the antioxidant N-acetylcysteine (NAC), for 4 weeks. Animals were sacrificed and various parameters (including mitochondrial bioenergetics) from liver, heart and kidney were evaluated

No significant differences were found in typical hepatic injury serum markers, showing that AgNPs toxicity is a silent phenomenon. However, mitochondria isolated from animals exposed to a very low dose of AgNPs showed a significant increase on reactive oxygen species (ROS) generation. Moreover, AgNPs caused impairment of rat liver mitochondrial function, mainly due to alterations of mitochondrial membrane permeability leading to an uncoupling effect on the oxidative phosphorylation system. AgNPs also compromised the electron transfer along the electron transport chain by affecting the activity of complexes II and IV of the respiratory chain and interfered with the mitochondrial permeability transition (MPT) induction. We found that most of the effects caused by AgNPs exposure were prevented by pretreatment with N-acetylcysteine (NAC), which highlights the crucial role of oxidative stress in AgNPs’ toxicity.

In summary, our results indicate that the liver is a target of AgNPs exposure leading to alteration in hepatic mitochondria functions. Thus, the mitochondrial toxicity may have a central role in the toxicity resulting from exposure to silver nanoparticles. The efficiency of NAC administration against AgNPs toxicity suggests that ROS are involved in the mitochondrial toxicity caused by AgNPs treatment.


Bioblast editor: Plangger M O2k-Network Lab: PT Coimbra Laranjinha J


Labels: MiParea: Respiration, Pharmacology;toxicology 

Stress:Permeability transition  Organism: Rat  Tissue;cell: Heart, Liver, Kidney 



HRR: Oxygraph-2k  Event: C1, Oral 


Affiliations

Uni Coimbra, Dept Life Sciences Fac Sciences & Technology, Coimbra, Portugal. - rsilva@uc.pt