AbstractsBiology & Animal Science

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. Over the last years there has been a rapid development of the nanotechnology industry and the inevitable human exposure tends rapidly to expand, accompanied by potential for adverse health effects. Among all used nanoparticles (NPs), silver nanoparticles (AgNPs) have the highest level of commercialization. Silver has been used for decades in medical healthcare due to its known antibacterial properties. One can also observe AgNPs in products used daily such as cosmetics, lotions, toothpastes, soaps, sunscreen, clothing and electronics. Over the last years, nanoparticles have been the subject of intense research for use in biomedicine, namely as biosensors, drug-delivery agents and imaging contrast agents, which take advantage of their unique optical properties. Human exposure to AgNPs can occur through different ways: inhalation, ingestion, injection and dermal contact. As a major organ of detoxification, the liver is one of the most important targets after AgNPs exposure. 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. The mechanism by which AgNPs cause toxicity is still subject to uncertainty. However, oxidative stress has been related with the AgNPs toxicity. Therefore, antioxidant therapy might be a viable strategy for attenuating this toxicity. In this work, we evaluated the toxicity of silver nanoparticles (10- and 75 nm) and their effects in rat liver mitochondrial bioenergetics. In vivo exposure to AgNPs was capable of increasing plasmatic aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) activities, suggesting hepatocellular injury. Mitochondria isolated from animals treated with both AgNPs sizes 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 byaffecting 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). This antioxidant agent efficiently prevented the structural damage in the inner mitochondrial membrane as well as damage to mitochondrial electron transport chain complexes. Oxidative phosphorylation and calcium retention capacities of hepatic mitochondria were also improved by NAC treatment. The…