Cognitive impairment, depressive-like behaviors and hippocampal microglia activation following exposure to air pollution nanoparticles.

Air pollution particulate matter (PM) is a world risk factor that the effects of long-term exposure to these factors in terms of damage to cardiovascular and pulmonary function are well known, but little is known comparatively about the effects of PM on emotional and cognitive processes. Exposure to PM can adversely affect the central nervous system (CNS) by inflammatory pathways and activation of reactive oxygen species (ROS) associated with urban air pollution PM. Therefore, we investigated whether prolonged exposure to diesel exhaust particles (DEPs) affects hippocampal inflammatory cytokines and emotional and cognition responses. Male mice were exposed to DEPs for 6 and 12 weeks. DEP-exposed mice indicated more disorders in depressive-like responses and spatial memory and learning than in control groups. Pro-inflammatory cytokine expression in tge hippocampus was increased among mice exposed to DEPs. The number of activated microglia increased in the dentate gyrus (DG) and CA1 regions of the hippocampus in DEP-exposed mice. These results show that chronic exposure to DEPs can alter neurobehavioral and impair cognition. Generally, these findings reaffirm the importance of protecting from exposure to ambient PM2.5 and also advance our understanding of the toxic actions of air pollution nanoparticles.

Mold and Mycotoxin Exposure and Brain Disorders.

Gene-environment interaction is an emerging hypothesis to explain the increased incidence of neurological disorders. In this context, the health and clinical effects of exposure to air pollutants have received increasing attention. One of these pollutants is the growth of fungi and molds in the form of multicellular filaments, known as hyphae. Fungi and molds not only grow in outdoor environments, but they also thrive indoors with excessive moisture, producing mycotoxins. Mold enters the body through the nose via the olfactory neurons, which directly communicate with the brain. Mycotoxins induce toxicological effects similar to those associated with brain disorders such as oxidative stress and inflammation. One mold species can produce several different mycotoxins, and one mycotoxin can be produced by several different molds. Even a small amount of mold growth in the air conditioners and their ducts or the panels inside the buildings and even the cars cause the occupants to be chronically exposed to and constantly inhaling spores and mycotoxins, which causes illness. In this review, we focused on mold and mycotoxin exposure and brain disorders.

Exposure to urban air pollution particulate matter: neurobehavioral alteration and hippocampal inflammation.

Air pollution is associated with many neurodevelopmental and neurological disorders in human populations. Rodent models show similar neurotoxic effects of urban air pollution ultrafine particulate matter (UFPs < 100 nm (PM0.1)), collected by different methods or from various sources. Exposure to ultrafine particulate matter (UFPs < 100 nm (PM0.1)) can be adversely impacting the central nervous system (CNS) by the activation of proinflammatory pathways and reactive oxygen species associated with air pollution particulate matter. We investigated hippocampal inflammatory cytokines, neurobehavioral alteration, and neuronal morphology following exposure to diesel exhaust particles (DEPs) in mice. Male mice were DEPs exposed for 14 weeks. Mice exposed to DEPs showed more disorders in spatial memory and learning and depressive-like responses than control mice. Expression of hippocampal pro-inflammatory cytokine was increased among DEPs exposure mice. The density of neurons in hippocampus CA1, CA3, and dentate gyrus (DG) regions decreased in DEPs mice. Overall, these findings show that prolonged exposure to DEPs in the world's major cities can alter neurobehavioral and impair cognition.

Airborne aerosols particles and COVID-19 transition.

With the outbreak of Coronavirus (2019) (COVID-19), as of late March 2020, understanding how the cause of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) transmitted is one of the most important questions that researchers are seeking to answer; because this effort helps to reduce the spread of disease. The COVID-19 is highly transmissible and deadly. Despite "tracking the call" and carefully examining patient contact, it is not yet clear how the virus is transmitted from one sick person to another. Why it is so transmissible? Can viruses be transmitted through speech and exhalation aerosols? How far can these aerosols go? How long can an aerosol containing a virus stay in the air? Is the virus amount in these aerosols enough to lead to an infection? There is no consensus on aerosols' role in the transmission of SARS-CoV-2. Findings show that SARS-CoV-2 aerosol transmission is possible. Therefore, to effectively reduce SARS-CoV-2, precautionary control strategies for aerosol transfer should be considered. Our aim is to review the evidence of the aerosol transmission containing SARS-CoV-2.

Investigation of metabolic kinetics in different brain regions of awake rats using the [1H-13C]-NMR technique.

Energy metabolism and neurotransmission are necessary for sustaining normal life activities. Hence, neurological or psychiatric disorders are always associated with changes in neurotransmitters and energy metabolic states in the brain. Most studies have only focused on the most important neurotransmitters, particularly GABA and Glu, however, other metabolites such as NAA and aspartate which are also very important for cerebral function are rarely investigated. In this study, most of the metabolic kinetics information of different brain regions was investigated in awake rats using the [1H-13C]-NMR technique. Briefly, rats (n = 8) were infused [1-13C] glucose through the tail vein for two minutes. After 20 min of glucose metabolism, the animals were sacrificed and the brain tissue was extracted and treated. Utilizing the 1H observed/13C-edited nuclear magnetic resonance (POCE-NMR), the enrichment of neurochemicals was detected which reflected the metabolic changes in different brain regions and the metabolic connections between neurons and glial cells in the brain. The results suggest that the distribution of every metabolite differed from every brain region and the metabolic rate of NAA was relatively low at 8.64 ± 2.37 µmol/g/h. In addition, there were some correlations between several 13C enriched metabolites, such as Glu4-Gln4 (p = 0.062), Glu4-GABA2 (p < 0.01), Glx2-Glx3 (p < 0.001), Asp3-NAA3 (p < 0.001). This correlativity reflects the signal transmission between astrocytes and neurons, as well as the potential interaction between energy metabolism and neurotransmission. In conclusion, the current study systematically demonstrated the metabolic kinetics in the brain which shed light on brain functions and the mechanisms of various pathophysiological states.

Learning and memory disorders related to hippocampal inflammation following exposure to air pollution.

It has been demonstrated that sub-chronic exposure to air pollution containing nanoscale (˂100 nm) diesel exhaust particles (DEPs) may lead to excessive oxidative stress and neuro-inflammation in adult male mice. Hereby, we investigated the effects of DEPs on hippocampus-dependent spatial learning and neuro-inflammation and memory-related gene expression in male mice. In this study, we divided 48 adult NMRI male mice into control group VS. three exposure groups. Mice were exposed to 300-350 µg/m3 DEPs for 2, 5, and 7 h daily for 12 weeks. The Morris Water Maze (MWM) and Elevated Plus Maze device were used to examine anxiety, spatial memory and learning, respectively. The mRNAs expression of pro-inflammatory cytokines, N-methyl-D-aspartate (NMDA) receptor subunits, and glutaminase were studied in hippocampus (HI) by real-time RT-PCR. Besides, malondialdehyde (MDA) tests were used to determine the state of oxidative stress. After 5 and 7 h. of DEPs exposure, mRNA expression of NR2A and NR3B IL1α, IL1ß, TNFα, NMDA receptor subunits and MDA levels increased significantly (P < 0.05). Also, DEPs exposed mice for 2, 5, and 7 h. showed diminished entrance into open arms with short time spent there. Indeed, 5 and 7 h/day exposed mice required a longer time to reach the hidden platform. Sub-chronic exposure to DEPs increased oxidative stress markers, neuroinflammation, anxiety, impaired spatial learning and memory.

Hippocampal inflammation and oxidative stress following exposure to diesel exhaust nanoparticles in male and female mice.

Air pollution exposure is among the most prevalent reasons for environmentally-induced oxidative stress and inflammation, both of which are involved in the development and progression of central nervous system (CNS) diseases. Ultrafine particles (UFPs) plays an important role in global air pollution and the diesel exhaust particles (DEPs) are the most important component in this regard. There are more than 40 toxic air pollutants in diesel exhaust (DE), which is one of the main constituents of an environmental pollutant and including particulate matter (PM) especially UFPs. Thus, in this study, adult female and male NMRI mice were exposed to DEPs (350-400 µg/m3) for 14 weeks (6 h per day and 5 days per week). After 14 weeks of exposure, expression of pro-inflammatory cytokines (IL-1α, IL-1ß, IL-6, TNF-α), nNOS, HO1, NR2A, and NR2B and malondialdehyde (MDA) level were analyzed in various brain regions such as the hippocampus (HI) and olfactory bulb (OB). Exposure to DEPs caused neuroinflammation and oxidative stress in female and male mice. That these effects observed in females were less pronounced than in male mice. The male mice emerged to be more susceptible significantly than the female mice to induced neuroinflammation following DEPs exposure. Also, our findings indicate that long term exposure to DEPs results in altered expression of hippocampal NMDA receptor subunits, and suggests that gender can play important role in the modulating susceptibility to neurotoxicity induced by DEPs exposure.

Prenatal exposure to diesel exhaust particles causes anxiety, spatial memory disorders with alters expression of hippocampal pro-inflammatory cytokines and NMDA receptor subunits in adult male mice offspring.

Air pollution by Diesel exhaust (DE) consists of gaseous compounds and diesel exhaust particles (DEPs). Previous studies show associations between prenatal exposure to diesel exhaust affects the central nervous system (CNS). However, there was not reported that these effects were caused by gaseous compounds, diesel exhaust particles, or both. A limited number of studies in rodent models have shown that exposure to DEPs can result in CNS. Here, we explored the effects of prenatal exposure to DEPs on anxiety and learning and memory in NMRI mice male offspring. Three groups of pregnant mice were exposed to 350-400 µg DEPs/m3 for 2, 4 and 6 h daily in a closed system room. We examined anxiety and learning and memory in 8-to-9-week-old male offspring using the Elevated plus maze and Morris water maze (MWM) test. Hippocampi were isolated after the behavioral tests and measured pro-inflammatory cytokines and N-methyl-D-aspartate (NMDA) receptor expression by quantitative RT-PCR analysis. Mice exposed to DEPs in utero showed deficits in the Elevated plus maze and Morris water maze test. In addition, DEPs exposed mice exhibited decreased hippocampal NR2A and NR3B expression. Taken together, our data suggest that maternal DEP exposure is associated with anxiety, disrupts learning and memory and reduction hippocampal NR2A and NR3B expression in male offspring.

Exposure to nanoscale diesel exhaust particles: Oxidative stress, neuroinflammation, anxiety and depression on adult male mice.

Exposure to nanoscale diesel engines exhausted particles (DEPs) is a well-recognized risk factor for respiratory and cardiovascular diseases. Rodents as commonly used models for urban air pollution in health effect studies demonstrate constant stimulation of inflammatory responses in the main areas of the brain. Nevertheless, the primary effect of diesel exhaust particulate matter on some of the brain regions and relation by behavioral alterations still remains untouched. We evaluated the brain regional inflammatory responses to a nanosized subfraction of diesel engines exhaust particulate matter (DEPs < 200 nm) in an adult male mice brain. Adult male mice were exposed to DEPs for 3, 6, and 8 h per day, 12 weeks and five days per week. Degree of anxiety and the depression by elevated plus maze and Forced Swimming Test respectively (FST) did measurement. After behavior tests, the plasma and some of the brain regions such as olfactory bulb (OB) and hippocampus (HI) were analyzed for oxidative stress and inflammatory responses. The inflammation and oxidative stress changes in OB and HI, markedly coincides with the results of behavioral alterations. These responses corresponded with rapid induction of MDA and nitrite oxide (NO) in brain regions and neuronal nitric oxide synthase (nNOS) mRNA followed by IL6, IL1α, and TNFα in OB and HI. The different times of DEPs exposure, leads to oxidative stress and inflammatory in plasma and brain regions. That this cumulative transport of inhaled nanoscale DEPs into the brain and creating to inflammation responses of brain regions may cause problems of brain function and anxiety and depression.