Ascorbic Acid Supplementation Prevents the Detrimental Effects of Prenatal and Postnatal Lead Exposure on the Purkinje Cell and Related Proteins in the Cerebellum of Developing Rats

Autor: Jin Seok Seo, Sung Min Nam, Tae-Hun Go, Sang-Soep Nahm, Byung-Joon Chang
Rok vydání: 2018
Předmět:
Male
medicine.medical_specialty
Cerebellum
Antioxidant
Endocrinology
Diabetes and Metabolism
medicine.medical_treatment
Clinical Biochemistry
Glutamate decarboxylase
Purkinje cell
Synaptophysin
Administration
Oral
Ascorbic Acid
010501 environmental sciences
Receptors
N-Methyl-D-Aspartate
01 natural sciences
Biochemistry
Rats
Sprague-Dawley
Inorganic Chemistry
Purkinje Cells
03 medical and health sciences
Glutamatergic
Internal medicine
medicine
Animals
gamma-Aminobutyric Acid
0105 earth and related environmental sciences
0303 health sciences
Glutamate Decarboxylase
Superoxide Dismutase
Chemistry
030302 biochemistry & molecular biology
Biochemistry (medical)
Neurotoxicity
General Medicine
medicine.disease
Ascorbic acid
Rats
medicine.anatomical_structure
Endocrinology
Lead
Cerebellar cortex
Female
Disks Large Homolog 4 Protein
Zdroj: Biological Trace Element Research. 190:446-456
ISSN: 1559-0720
0163-4984
DOI: 10.1007/s12011-018-1572-y
Popis: We investigated the effects of lead (Pb) and ascorbic acid co-administration on rat cerebellar development. Prior to mating, rats were randomly divided into control, Pb, and Pb plus ascorbic acid (PA) groups. Pregnant rats were administered Pb in drinking water (0.3% Pb acetate), and ascorbic acid (100 mg/kg) via oral intubation until the end of the experiment. Offspring were sacrificed at postnatal day 21, the age at which the morphology of the cerebellar cortex in developing pups is similar to that of the adult brain. In the cerebellum, Pb exposure significantly reduced Purkinje cells and ascorbic acid prevented their reduction. Along with the change of the Purkinje cells, long-term Pb exposure significantly reduced the expression of the synaptic marker (synaptophysin), γ-aminobutyric acid (GABA)-synthesizing enzyme (glutamic acid decarboxylase 67), and axonal myelin basic protein while ascorbic acid co-treatment attenuated Pb-mediated reduction of these proteins in the cerebellum of pups. However, glutamatergic N-methyl-D-aspartate receptor subtype 1 (NMDAR1), anchoring postsynaptic density protein 95 (PSD95), and antioxidant superoxide dismutases (SODs) were adversely changed; Pb exposure increased the expression of NMDAR1, PSD95, and SODs while ascorbic acid co-administration attenuated Pb-mediated induction. Although further studies are required about the neurotoxicity of the Pb exposure, the results presented here suggest that developmental Pb exposure disrupted normal development of Purkinje cells by increasing glutamatergic and oxidative stress in the cerebellum. Additionally, ascorbic acid co-treatment is beneficial in attenuating prenatal and postnatal Pb exposure-induced maldevelopment of Purkinje cells in the developing cerebellum.
Databáze: OpenAIRE
Externí odkaz: