Methylmercury intoxication and cortical ischemia: Pre-clinical study of their comorbidity

Autor: Walace Gomes-Leal, Luana Ketlen Reis Leão, Luana N. S. Santana, Maria Elena Crespo-Lopez, Lílian Lund Amado, Rafael Rodrigues Lima, Leonardo Oliveira Bittencourt, Márcia Cristina Freitas da Silva, Luanna Melo Pereira Fernandes, Marco Aurelio M. Freire, Rafael Monteiro Fernandes, Priscila Cunha Nascimento, Cristiane Socorro Ferraz Maia
Rok vydání: 2018
Předmět:
Male
medicine.medical_specialty
Health
Toxicology and Mutagenesis
0211 other engineering and technologies
Ischemia
02 engineering and technology
Oxidative phosphorylation
Comorbidity
010501 environmental sciences
medicine.disease_cause
01 natural sciences
Brain Ischemia
Lipid peroxidation
chemistry.chemical_compound
Internal medicine
medicine
Animals
Rats
Wistar
Methylmercury
Neuroinflammation
0105 earth and related environmental sciences
Neurons
021110 strategic
defence & security studies
business.industry
Public Health
Environmental and Occupational Health
Motor Cortex
Brain
General Medicine
Methylmercury Compounds
medicine.disease
Pollution
Motor coordination
Rats
Stroke
Oxidative Stress
medicine.anatomical_structure
Endocrinology
chemistry
Lipid Peroxidation
business
Oxidative stress
Motor cortex
Zdroj: Ecotoxicology and environmental safety. 174
ISSN: 1090-2414
Popis: Stroke is one of the main causes of human disability worldwide. Ischemic stroke is mostly characterized by metabolic collapse and fast tissue damage, followed by secondary damage in adjacent regions not previously affected. Heavy metals intoxication can be associated with stroke incidence, because of their damaging action in the vascular system. Mercury, in particular, possesses a high tropism by metabolically active regions, such as the brain. In the present study we sought to evaluate whether methylmercury (MeHg) intoxication can aggravate the tissue damage caused by an ischemic stroke induced by microinjections of endothelin-1 (ET-1) into the motor cortex of adult rats. Following MeHg intoxication by gavage (0.04 mg/kg/day) during 60 days, the animals were injected with ET-1 (1 μl, 40 pmol/μl) or vehicle (1 μl). After 7 days, all animals were submitted to behavioral tests and then their brains were processed to biochemical and immunohistochemical analyses. We observed that long-term MeHg intoxication promoted a significant Hg deposits in the motor cortex, with concomitant increase of microglial response, followed by reduction of the neuronal population following ischemia and MeHg intoxication, as well as disturbance in the antioxidant defense mechanisms by misbalance of oxidative biochemistry with increase of both lipid peroxidation and nitrite levels, associated to behavioral deficits. MeHg exposure and cortical ischemia demonstrated that both injuries are able of causing significant neurobehavioural impairments in motor coordination and learning accompanied of an exacerbated microglial activation, oxidative stress and neuronal loss in the motor cortex, indicating that MeHg as a source of metabolic disturbance can act as an important increasing factor of ischemic events in the brain.
Databáze: OpenAIRE
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