Low doses of methylmercury exposure during adulthood in rats display oxidative stress, neurodegeneration in the motor cortex and lead to impairment of motor skills

Santana, Luana Nazaré da Silva; Bittencourt, Leonardo Oliveira; Nascimento, Priscila Cunha; Fernandes, Rafael M.; Teixeira, Francisco Bruno; Fernandes, Luanna Melo Pereira; Silva, Márcia Cristina Freitas; Amado, Lílian Lund; Crespo-López, María Elena; Maia, Cristiane do Socorro Ferraz; Lima, Rafael Rodrigues

doi:10.1016/j.jtemb.2018.09.004

Cited by 52 publications

(32 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…After antigen retrieval, they were immersed in PBS for 10 min and immersed in methanol-hydrogen peroxide solution (3:100, v/v) for endogenous peroxidase inhibition. Anti-NeuN (1:100, Chemicon), Anti-Myelin Basic Protein (MBP) (1:250, Promega) and Anti-Synaptophysin (1:1000, Wako) antibodies for immunolabeling of neurons, as well as MPB and synaptic vesicles, respectively, as previously established by our group were applied [22,75,76]. Revelation was proceeded by 3,3 -diaminobenzidine solution in PBS; sections immunolabeled with anti-MBP and anti-Synaptophysin were counter stained with Mayer's hematoxylin.…”

Section: Immunohistochemical Assaysmentioning

confidence: 99%

“…For analyses of anti-MBP and anti-Synaptophysin immunostaining, we first obtained the photomicrographs using the microscope Nikon Eclipse E500 with Moticam 2500 ® attached to it. The photomicrographs were analyzed using ImageJ software with Color Deconvolution plugin according to previous works from our group [75,76], which extracted the fraction of area immunolabeled by the antibodies and revealed by DAB. The results are expressed as fraction of area (%) immunolabeled in comparison to the total area of section captured by the camera system.…”

Section: Quantitative Analyses Of Immunohistochemistry Assaysmentioning

confidence: 99%

See 1 more Smart Citation

Long-Term Lead Exposure Since Adolescence Causes Proteomic and Morphological Alterations in the Cerebellum Associated with Motor Deficits in Adult Rats

Leão

Bittencourt

Oliveira

et al. 2020

IJMS

Self Cite

View full text Add to dashboard Cite

Lead (Pb) is an environmental contaminant that presents a high risk for human health. We aimed to investigate the possible alterations triggered by the exposure to Pb acetate for a long period in motor performance and the possible relationship with biochemical, proteomic and morphological alterations in the cerebellum of rats. Male Wistar rats were exposed for 55 days, at 50 mg/Kg of Pb acetate, and the control animals received distilled water. Open field (OF) and rotarod tests; biochemistry parameters (MDA and nitrite); staining/immunostaining of Purkinje cells (PC), mature neurons (MN), myelin sheath (MS) and synaptic vesicles (SYN) and proteomic profile were analyzed. Pb deposition on the cerebellum area and this study drove to exploratory and locomotion deficits and a decrease in the number of PC, MN, SYN and MS staining/immunostaining. The levels of MDA and nitrite remained unchanged. The proteomic profile showed alterations in proteins responsible for neurotransmitters release, as well as receptor function and second messengers signaling, and also proteins involved in the process of apoptosis. Thus, we conclude that the long-term exposure to low Pb dose promoted locomotion and histological tracings, associated with alterations in the process of cell signaling, as well as death by apoptosis.

show abstract

Section: Immunohistochemical Assaysmentioning

confidence: 99%

Section: Quantitative Analyses Of Immunohistochemistry Assaysmentioning

confidence: 99%

Long-Term Lead Exposure Since Adolescence Causes Proteomic and Morphological Alterations in the Cerebellum Associated with Motor Deficits in Adult Rats

Leão

Bittencourt

Oliveira

et al. 2020

IJMS

Self Cite

View full text Add to dashboard Cite

show abstract

“…To investigate the possible neuronal death triggered in this experimental model, 24 h of behavioral assays, 9 animals from each group were randomly selected and submitted to perfusion, histological processing and immunohistochemical evaluation for immunostaining of mature neurons in the hippocampus. For this investigation, we selected the anti-NeuN marking, previously described in our studies [18,71]. For this, they were anesthetized with ketamine hydrochloride (90 mg/kg) and xylazine hydrochloride (9 mg/kg) and perfused through the left ventricle of the heart with 0.9% heparinized saline solution, followed by 4% paraformaldehyde.…”

Section: Perfusion Histological and Immunohistochemistry Proceduresmentioning

confidence: 99%

Hippocampal Impairment Triggered by Long-Term Lead Exposure from Adolescence to Adulthood in Rats: Insights from Molecular to Functional Levels

Oliveira

Dionízio

Teixeira

et al. 2020

IJMS

Self Cite

View full text Add to dashboard Cite

Lead (Pb) is an environmental and occupational neurotoxicant after long-term exposure. This study aimed to investigate the effects of systemic Pb exposure in rats from adolescence to adulthood, evaluating molecular, morphologic and functional aspects of hippocampus. For this, male Wistar rats were exposed to 50 mg/kg of Pb acetate or distilled water for 55 days by intragastric gavage. For the evaluation of short-term and long-term memories, object recognition and step-down inhibitory avoidance tests were performed. At the end of the behavioral tests, the animals were euthanized and the hippocampus dissected and processed to the evaluation of: Pb content levels in hippocampal parenchyma; Trolox equivalent antioxidant capacity (TEAC), glutathione (GSH) and malondialdehyde (MDA) levels as parameters of oxidative stress and antioxidant status; global proteomic profile and neuronal degeneration by anti-NeuN immunohistochemistry analysis. Our results show the increase of Pb levels in the hippocampus of adult rats exposed from adolescence, increased MDA and GSH levels, modulation of proteins related to neural structure and physiology and reduced density of neurons, hence a poor cognitive performance on short and long-term memories. Then, the long-term exposure to Pb in this period of life may impair several biologic organizational levels of the hippocampal structure associated with functional damages.

show abstract

“…All immunohistochemistry procedures were conducted according to the previously published studies [34–36]. Briefly, sections were dewaxed in xylene, hydrated in decreasing ethanol solutions (absolute 2, absolute 1, 90%, 80%, 70%), and rinsed in 0.1 M PBS for 5 min.…”

Section: Methodsmentioning

confidence: 99%

Physical Exercise Attenuates Oxidative Stress and Morphofunctional Cerebellar Damages Induced by the Ethanol Binge Drinking Paradigm from Adolescence to Adulthood in Rats

Lamarão-Vieira

Pamplona-Santos

Nascimento

et al. 2019

Oxidative Medicine and Cellular Longevity

Self Cite

View full text Add to dashboard Cite

Ethanol (EtOH) binge drinking is characterized by high EtOH intake during few hours followed by withdrawal. Protection strategies against the damages generated by this binge are poorly explored. Thus, this study is aimed at investigating the protective role of treadmill physical exercise (PE) on the damage caused after repeated cycles of binge-like EtOH exposure in the oxidative biochemistry, morphology, and cerebellar function of rats from adolescence to adulthood. For this, animals were divided into four groups: control group (sedentary animals with doses of distilled water), exercised group (exercised animals with doses of distilled water), EtOH group (sedentary animals with doses of 3 g/kg/day of EtOH, 20% w/v), and exercised+EtOH group (exercised animals with previous mentioned doses of EtOH). The PE occurred on a running treadmill for 5 days a week for 4 weeks, and all doses of EtOH were administered through intragastric gavage in four repeated cycles of EtOH in a binge-like manner. After the EtOH protocol and PE, animals were submitted to open field and beam walking tests. In sequence, the cerebellums were collected for the biochemical and morphological analyses. Biochemical changes were analyzed by measurement of Trolox equivalent antioxidant capacity (TEAC), reduced glutathione content measurements (GSH), and measurement of nitrite and lipid peroxidation (LPO). In morphological analyses, Purkinje cell density evaluation and immunohistochemistry evaluation were measured by antimyelin basic protein (MBP) and antisynaptophysin (SYP). The present findings demonstrate that the binge drinking protocol induced oxidative biochemistry misbalance, from the decrease of TEAC levels and higher LPO related to tissue damage and motor impairment. In addition, we have shown for the first time that treadmill physical exercise reduced tissue and functional alterations displayed by EtOH exposure.

show abstract

Low doses of methylmercury exposure during adulthood in rats display oxidative stress, neurodegeneration in the motor cortex and lead to impairment of motor skills

Cited by 52 publications

References 67 publications

Long-Term Lead Exposure Since Adolescence Causes Proteomic and Morphological Alterations in the Cerebellum Associated with Motor Deficits in Adult Rats

Long-Term Lead Exposure Since Adolescence Causes Proteomic and Morphological Alterations in the Cerebellum Associated with Motor Deficits in Adult Rats

Hippocampal Impairment Triggered by Long-Term Lead Exposure from Adolescence to Adulthood in Rats: Insights from Molecular to Functional Levels

Physical Exercise Attenuates Oxidative Stress and Morphofunctional Cerebellar Damages Induced by the Ethanol Binge Drinking Paradigm from Adolescence to Adulthood in Rats

Contact Info

Product

Resources

About