Exposure to Benzo[a]pyrene Decreases Noradrenergic and Serotonergic Axons in Hippocampus of Mouse Brain

被引:4
|
作者
Abd El Naby, Walaa Slouma Hamouda [1 ,2 ]
Zong, Cai [1 ]
Fergany, Alzahraa [1 ,2 ]
Ekuban, Frederick Adams [1 ,3 ]
Ahmed, Saleh [1 ]
Reda, Yousra [1 ]
Sato, Harue [1 ]
Ichihara, Sahoko [4 ]
Kubota, Natsuko [5 ]
Yanagita, Shinya [5 ]
Ichihara, Gaku [1 ]
机构
[1] Tokyo Univ Sci, Fac Pharmaceut Sci, Dept Occupat & Environm Hlth, Noda 2788510, Japan
[2] Alexandria Univ, Fac Vet Med, Dept Anim Husb & Anim Wealth Dev, Genet & Genet Engn, Alexandria 21500, Egypt
[3] Univ Louisville, Dept Med Pharmacol & Toxicol, Div Gastroenterol Hepatol & Nutr, Louisville, KY 40202 USA
[4] Jichi Med Univ, Dept Environm & Prevent Med, Shimotsuke 3290498, Japan
[5] Tokyo Univ Sci, Fac Sci & Technol, Noda 2788510, Japan
基金
日本学术振兴会;
关键词
benzo[a]pyrene; neurotoxicity; noradrenergic axons; serotonergic axons; genes expression; AUTONOMIC NERVOUS-SYSTEM; NEUROBEHAVIORAL FUNCTION; GENE-EXPRESSION; RAT; BEHAVIOR; CELLS;
D O I
10.3390/ijms24129895
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Epidemiological studies showed the association between air pollution and dementia. A soluble fraction of particulate matters including polycyclic aromatic hydrocarbons (PAHs) is suspected to be involved with the adverse effects of air pollution on the central nervous system of humans. It is also reported that exposure to benzopyrene (B[a]P), which is one of the PAHs, caused deterioration of neurobehavioral performance in workers. The present study investigated the effect of B[a]P on noradrenergic and serotonergic axons in mouse brains. In total, 48 wild-type male mice (10 weeks of age) were allocated into 4 groups and exposed to B[a]P at 0, 2.88, 8.67 or 26.00 & mu;g/mice, which is approximately equivalent to 0.12, 0.37 and 1.12 mg/kg bw, respectively, by pharyngeal aspiration once/week for 4 weeks. The density of noradrenergic and serotonergic axons was evaluated by immunohistochemistry in the hippocampal CA1 and CA3 areas. Exposure to B[a]P at 2.88 & mu;g/mice or more decreased the density of noradrenergic or serotonergic axons in the CA1 area and the density of noradrenergic axons in the CA3 area in the hippocampus of mice. Furthermore, exposure to B[a]P dose-dependently upregulated Tnf & alpha; at 8.67 & mu;g/mice or more, as well as upregulating Il-1 & beta; at 26 & mu;g/mice, Il-18 at 2.88 and 26 & mu;g/mice and Nlrp3 at 2.88 & mu;g/mice. The results demonstrate that exposure to B[a]P induces degeneration of noradrenergic or serotonergic axons and suggest the involvement of proinflammatory or inflammation-related genes with B[a]P-induced neurodegeneration.
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页数:13
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