We and other groups have demonstrated that exposure to nickel nanoparticles (Nano-Ni) results in severe and persistent lung inflammation and fibrosis, but the underlying mechanisms remain unclear. Here, we propose that miR-21 may play an important role in Nano-Ni-induced lung inflammation, injury, and fibrosis. Our dose-and time-response studies demonstrated that exposure of C57BL/6J (WT) mice to Nano-Ni resulted in upregulation of miR-21, proinflammatory cytokines, and profibrotic mediators. Histologically, exposure to Nano-Ni caused severe pulmonary inflammation and fibrosis. Based on the dose-and time-response studies, we chose a dose of 50 μg of Nano-Ni per mouse to compare the effects of Nano-Ni on WT with those on miR-21 KO mouse lungs. At day 3 post-exposure, Nano-Ni caused severe acute lung inflammation and injury that were reflected by increased neutrophil count, CXCL1/KC level, LDH activity, total protein concentration, MMP-2/9 protein levels and activities, and proinflammatory cytokines in the BALF or lung tissues from WT mice, which were confirmed histologically. Although Nano-Ni had similar effects on miR-21 KO mice, the above mentioned levels were significantly lower than those in WT mice. Histologically, lungs from WT mice exposed to Nano-Ni had infiltration of a large number of polymorphonuclear (PMN) cells and macrophages in the alveolar space and interstitial tissues. However, exposure of miR-21 KO mice to Nano-Ni only caused mild acute lung inflammation and injury. At day 42 post-exposure, Nano-Ni caused extensive pulmonary fibrosis and chronic inflammation in the WT mouse lungs. However, exposure of miR-21 KO mice to Nano-Ni only caused mild lung fibrosis and chronic lung

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Background Cooking oil fumes (COFs) are composed of particulate matter, polycyclic aromatic hydrocarbons, volatile organic compounds, aldehydes, and ketones, and are currently a global health concern. Some agents in COFs are mutagenic and carcinogenic. However, only a few reports have addressed the hazardous effects of COF exposure on the female reproductive system. In this study, we explored the effects of subchronic exposure to COFs on female gonads in vivo and the possible involvement of the G-protein-coupled receptor 30 signaling pathway. Methods COFs were generated by heating commercially available canola oil in an iron pot. Adult female Wistar rats at 2 months of age were exposed to COFs at 32 mg/m 3 for 0, 0.5, 1, 2, or 4 h/day for 56 days. The estrous cycle in rats was studied twice at 7:00 a.m. and 7:00 p.m. on the 43rd treatment day until the current estrous cycle was complete. The rat body weight was measured before the experiment and at day 56 post-exposure. At the end of the experiment, rat blood was collected for gonadal hormone assay, and ovaries were collected for histology and mRNA isolation. The mRNA levels of GPR30, EGFR, STAT3, and ERK were determined by quantitative RT-PCR. Results At a concentration of 32.21 ± 5.11 mg/m3, COF exposure extended the estrous cycle in rats, and ovary coefficient decreased. COFs showed various effects on the sex hormone levels and follicles, depending on its exposure level. Exposure to COFs led to the changes in mRNA levels of the G-protein-coupled receptor 30 (GPR30), epidermal growth factor receptor (EGFR), signal transducer and activator of transcription 3 (STAT3), and extracellular signal-regulated kinase (ERK). Conclusion This study indicated that cooking oil fume exposure disrupted the estrous cycle, sex hormone patterns, and follicle development in female rats in a dose-dependent manner. These adverse effects of cooking oil fumes on female reproductive health were correlated with the G-protein-coupled receptor 30-mediated signaling pathway.

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