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Effects of exposure to nanoparticle-rich diesel exhaust on adrenocortical function in adult male mice

Li C, Li X, Suzuki AK, Fujitani Y, Jigami J, Nagaoka K, et al. Effects of exposure to nanoparticle-rich diesel exhaust on adrenocortical function in adult male mice. Toxicology Letters 2012;209:277–81.

Abstract

To investigate the effects of nanoparticle-rich diesel exhaust (NR-DE) on adrenocortical function, seven-week-old male mice were divided into four groups and exposed to either whole NR-DE at low (41.73 μg/m3, 8.21 × 105 particles/cm3), high (152.01 μg/m3, 1.80 × 106 particles/cm3) concentrations, filtered diesel exhaust (F-DE) or clean air for 8 weeks (5 h/day, 5 days/week). After 8 weeks of exposure, the animals were euthanized under pentobarbital anesthesia and the blood samples were collected to detect serum progesterone and corticosterone. In addition, adrenal glands were excised, and adrenal cells were cultured in the absence or presence of rat adrenocorticotropic hormone (ACTH) (10−15 to 10−10 M) for 4 h. There were no significant differences in the body weight, absolute and relative adrenal gland weight among the groups. Serum concentration of corticosterone and progesterone was not changed significantly. Administration of ACTH resulted in a dose-dependent increase in corticosterone and progesterone release in mice-exposed to low-concentration NR-DE and clean air. Moreover, corticosterone and progesterone concentrations in adrenal cells increased significantly in mice-exposed to low-concentration NR-DE basal and administrated with ACTH (10−15 to 10−11 M for corticosterone; 10−14 to 10−11 M for progesterone) compared with the control mice. In contrast, the concentration of corticosterone and progesterone decreased significantly in mice-exposed to high-concentration NR-DE or F-DE basal and administrated with ACTH (10−12 to 10−10 M for corticosterone; 10−15 to 10−10 M for progesterone) compared with the control mice. These results suggest that exposure to NR-DE or F-DE may disrupt adrenocortical function in adult male mice.