MRI and neuropathological validations of the involvement of air pollutants in cortical selective neuronal loss.
Vehicles are a major source of air pollution, especially particulate matter (PM) pollution, throughout the world and auto-rickshaws are considered main contributors to this air pollution. PM, in addition to causing respiratory and cardiovascular disorders, has potential to gain access to the brain and could induce neuroinflammation leading to different neurological disorders. Therefore, in the current project, MRI and immunohistochemistry techniques were adopted to ascertain the neurotoxic potential of the chronic exposure to different PM generated by two-stroke auto-rickshaws (TSA), four-stroke auto-rickshaws (FSA), and aluminum sulfate (AS) solution in rats. The results highlighted that all treated groups followed a pattern of dose-dependent increase in pure cortical neuronal loss, selective neuronal loss (SNL), nuclear pyknosis, karyolysis, and karyorrhexis. Mild to moderate areas of penumbra were also observed with increase in the population of activated microglia and astrocytes, while no alteration in the intensities of T2W MRI signals was perceived in any group. When comparing the findings, TSA possess more neurotoxic potential than FSA and AS, which could be associated with increased concentration of certain elements in TSA emissions. The study concludes that chronic exposure to PM from TSA, FSA, and AS solutions produces diverse neuropathies in the brain, which may lead to different life-threatening neurological disorders like stroke, Alzheimer's, and Parkinson's disorders. Government and environmental agencies should take serious notice of this alarming situation, and immediate steps should be implemented to improve the standards of PM emissions from auto-rickshaws.
Sohail
S
Ejaz
Khaleeq
K
Anwar
Muhammad
M
Ashraf
D000393:Air Pollutants / Q000633:toxicity*; D000534:Alum Compounds / Q000633:toxicity; D000818:Animals; D034961:Antigens, Nuclear / Q000378:metabolism; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D039481:CD11b Antigen / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D008279:Magnetic Resonance Imaging; D018986:Motor Vehicles; D009419:Nerve Tissue Proteins / Q000378:metabolism; D009474:Neurons / Q000187:drug effects* / Q000473:pathology; D052638:Particulate Matter / Q000633:toxicity*; D051381:Rats; D017208:Rats, Wistar; D001335:Vehicle Emissions / Q000633:toxicity*
D000393:Air Pollutants; D000534:Alum Compounds; D034961:Antigens, Nuclear; D039481:CD11b Antigen; D005904:Glial Fibrillary Acidic Protein; D009419:Nerve Tissue Proteins; D052638:Particulate Matter; C546339:Rbfox3 protein, rat; D001335:Vehicle Emissions; C041524:aluminum sulfate