Aluminum Nanoparticles Induce ERK and p38MAPK Activation in Rat Brain

Abstract

Aluminum nanoparticles (Al-NPs) are one of the most widely used nanomaterial in cosmetics and medical materials. For this reason, Al-NP exposure is very likely to occur via inhalation in the environment and the workplace. Nevertheless, little is known about the mechanism of Al-NP neurotoxicity via inhalation exposure. In this study, we investigated the effect AL-NPs on the brain. Rats were exposed to Al-NPs by nasal instillation at 1 mg/kg body weight (low exposure group), 20 mg/kg body weight (moderate exposure group), and 40 mg/kg body weight (high exposure group), for a total of 3 times, with a 24-hr interval after each exposure. Inductively coupled plasma mass spectrometry (ICP-MS) analysis indicated that the presence of aluminum was increased in a dose-dependent manner in the olfactory bulb (OFB) and the brain. In microarray analysis, the regulation of mitogen-activated protein kinases (MAPK) activity (GO: 0043405), including Ptprc, P2rx7, Map2k4, Trib3, Trib1, and Fgd4 was significantly over-expressed in the treated mice than in the controls (p = 0.0027). Moreover, Al-NPs induced the activation of ERK1 and p38 MAPK protein expression in the brain, but did not alter the protein expression of JNK, when compared to the control. These data demonstrate that the nasal exposure of Al-NPs can permeate the brain via the olfactory bulb and modulate the gene and protein expression of MAPK and its activity.

Application of dental nanomaterials: potential toxicity to the central nervous system

“…The authors further noted some significant changes in genes that may be potential biomarkers of brain toxicity. Similar findings were also reported by Kwon et al 72 who found that Al NPs exposure modulated the gene and protein expressions of mitogen-activated protein kinases and their activities. Marano et al 73 recently discussed the NP-induced reactive oxygen species (ROS) generation and activation of signaling pathways involving various protein kinases.…”

Interplay of glia activation and oxidative stress formation in fluoride and aluminium exposure

“…This could mean that intake of fluoride at this dose does not overwhelm the antioxidant system [1]. However, it is important to note that fluoride toxicity is not only determined by the amount of exposure but also by the duration of exposure [2,30]. Hence, accumulation of fluoride in the body over a very long duration may cause neurotoxic effects although more studies are required to confirm this hypothesis.…”

Activation of p38-mitogen-activated protein kinase contributes to ischemia reperfusion in rat brain

“…p38mapk is an intermediary between osteopontin and aldosterone, and is an inflammatory mediator that can destroy normal tissue (Fu et al, 2012). Kwon et al (2013) have demonstrated that aluminum nanoparticles have a neurotoxic effect on rat brains that is mediated by activation of the p38mapk pathway. Cellphone radiation exposure can lead to biological interaction, and 3G mobile phone exposure causes a transient increase in phosphorylation of p38mapk.…”