Adverse effects of subchronic exposure to cooking oil fumes on the gonads and the GPR30-mediated signaling pathway in female rats

Abstract

BackgroundCooking 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.MethodsCOFs 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/m3 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.ResultsAt 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).ConclusionThis 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.HighlightsSubchronic exposure to COFs for 56 days had gonadal toxicity in female rats, that disrupted the estrous cycle, sex hormone patterns, and follicle development in a dose-dependent manner.Reproductive endocrine disruption might be one of the female gonadotoxicity mechanisms of COFs.These adverse effects of COFs on female reproductive health were correlated with the GPR30-mediated signaling pathway.