title: Effect of nanoparticle-rich diesel exhaust on testosterone biosynthesis in adult male mice.
abstract: The effect of nanoparticle-rich diesel exhaust (NR-DE) on the testicular function and factors related with the biosynthesis of testosterone gene expression were investigated in mice. Male C57BL/Jcl mice were exposed to clean air, low-dose NR-DE (Low NR-DE), high-dose NR-DE (High NR-DE) or filtered diesel exhaust (F-DE) for 8 weeks. We found that the mice exposed to High NR-DE had significantly higher testosterone levels than those in the control and F-DE groups. To determine the effects of NR-DE on testicular testosterone production, interstitial cells dissected from the male mice which were exposed to NR-DE, F-DE, or clean air for 8 weeks were incubated with or without human chorionic gonadotropin (hCG; 0.1 IU/mL) for 4 h. The concentrations of testosterone in the culture media were measured. The testosterone production was significantly increased in with or without hCG of High NR-DE exposed group, and significantly decreased in both with or without hCG of F-DE exposed groups. Moreover, several genes, which is associated with testicular cholesterol synthesis, HMG-CoA, LDL-R, SR-B1, PBR, and P450scc, P450 17α, and 17β-HSD were determined in the testis of adult male mice. The results showed High NR-DE exposure significantly increased the expression of these genes. Whereas, the levels in the F-DE exposure group returned to those in the control group, implicating that the nanoparticles in DE contribute to the observed reproductive toxicity. We conclude that enhancement of testosterone biosynthesis by NR-DE exposure may be regulated by increasing testicular enzymes of testosterone biosynthesis.
authors.affiliation: College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China. chunmeili@njau.edu.cn
authors.forename: ChunMei
authors.initials: C
authors.lastname: Li
authors.forename: Xuezheng
authors.initials: X
authors.lastname: Li
authors.forename: Junko
authors.initials: J
authors.lastname: Jigami
authors.forename: Chisa
authors.initials: C
authors.lastname: Hasegawa
authors.forename: Akira K
authors.initials: AK
authors.lastname: Suzuki
authors.forename: Yonghui
authors.initials: Y
authors.lastname: Zhang
authors.forename: Yuji
authors.initials: Y
authors.lastname: Fujitani
authors.forename: Kentaro
authors.initials: K
authors.lastname: Nagaoka
authors.forename: Gen
authors.initials: G
authors.lastname: Watanabe
authors.forename: Kazuyoshi
authors.initials: K
authors.lastname: Taya
mesh_terms: D015067:17-Hydroxysteroid Dehydrogenases / Q000235:genetics; D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D002786:Cholesterol Side-Chain Cleavage Enzyme / Q000235:genetics; D005640:Follicle Stimulating Hormone / Q000097:blood; D006903:Hydroxymethylglutaryl CoA Reductases / Q000235:genetics; D006904:Hydroxymethylglutaryl-CoA Synthase / Q000235:genetics; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D053758:Nanoparticles / Q000633:toxicity*; D011374:Progesterone / Q000097:blood; D011963:Receptors, GABA-A / Q000235:genetics; D011973:Receptors, LDL / Q000235:genetics; D051122:Scavenger Receptors, Class B / Q000235:genetics; D013076:Sperm Count; D013254:Steroid 17-alpha-Hydroxylase / Q000235:genetics; D013737:Testis / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D013739:Testosterone / Q000096:biosynthesis* / Q000097:blood; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D000393:Air Pollutants; D011963:Receptors, GABA-A; D011973:Receptors, LDL; C454739:Scarb1 protein, mouse; D051122:Scavenger Receptors, Class B; D001335:Vehicle Emissions; D013739:Testosterone; D011374:Progesterone; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D015067:17-Hydroxysteroid Dehydrogenases; D006903:Hydroxymethylglutaryl CoA Reductases; D013254:Steroid 17-alpha-Hydroxylase; D002786:Cholesterol Side-Chain Cleavage Enzyme; D006904:Hydroxymethylglutaryl-CoA Synthase