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Biol Trace Elem Res

Title:		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
Author(s):		Nam SM; Seo JS; Go TH; Nahm SS; Chang BJ;
Address:		"Department of Anatomy, College of Veterinary Medicine, Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul, 05030, Republic of Korea. College of Veterinary Medicine and Veterinary Science Research Institute, Konkuk University, Seoul, 05030, Republic of Korea. Department of Anatomy, College of Veterinary Medicine, Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul, 05030, Republic of Korea. bjchang@konkuk.ac.kr. College of Veterinary Medicine and Veterinary Science Research Institute, Konkuk University, Seoul, 05030, Republic of Korea. bjchang@konkuk.ac.kr"
Journal Title:		Biol Trace Elem Res
Year:		2019
Volume:		20181128
Issue:		2
Page Number:		446 - 456
DOI:		10.1007/s12011-018-1572-y
ISSN/ISBN:		1559-0720 (Electronic) 0163-4984 (Linking)
Abstract:		"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), gamma-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"
Keywords:		"Administration, Oral Animals Ascorbic Acid/administration & dosage/*pharmacology Cerebellum/*drug effects/growth & development/metabolism Disks Large Homolog 4 Protein/metabolism Female Glutamate Decarboxylase/antagonists & inhibitors/metabolism Lead/admi;"
Notes:		"MedlineNam, Sung Min Seo, Jin Seok Go, Tae-Hun Nahm, Sang-Soep Chang, Byung-Joon eng 2018/11/30 Biol Trace Elem Res. 2019 Aug; 190(2):446-456. doi: 10.1007/s12011-018-1572-y. Epub 2018 Nov 28"