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Short-Chain Chlorinated Paraffins May Induce Ovarian Damage in Mice via AIM2- and NLRP12-PANoptosome
Mingxin Bai1, Jiawei Lei1, Fan Li1
1Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Preventive Medicine, Medical school, Hunan Normal University, Changsha, Hunan 410013, China.
Abstract:
Humans may intake 0.02 mg/kg/day of short-chain chlorinated paraffins (SCCPs), and no study is available on mammalian ovarian damage caused by low-level SCCPs. In this study, four groups of 5-week-old female Institute of Cancer Research (ICR) mice were orally administered 0, 0.01, 0.1, and 1.0 mg/kg/day SCCPs for 21 consecutive days, and serum and ovaries were collected 20 h after the last SCCPs-administration. SCCPs at ≥0.1 mg/kg/day were found to reduce follicle counts at each stage, induce dose-dependent oxidative stress in mice, and lower serum E2 and ovarian anti-Müllerian hormone levels. The data indicated that cellular PANoptosis increased in the ovaries of all SCCP-treated mice. Furthermore, AIM2- and NLRP12-PANoptosome gene and protein levels were considerably elevated. Female germline stem cells (FGSCs) in the cortical portion of the ovary exhibited substantial damage in all SCCP groups, additionally, the expression of FGSC marker genes and major marker proteins was diminished in the ovaries. Oral administration of SCCPs with 0.01, 0.1, and 1.0 mg/kg/day to mice resulted in PANoptosis of the ovaries. Therefore, it was suggested that the oral administration of ≥0.1 mg/kg/day of SCCPs suppressed ovarian function, which may be attributed to the fact that SCCPs induced the generation of AIM2- and NLRP12-PANoptosome in ovary cells.
Insights
Short-chain chlorinated paraffins (SCCPs) at doses of 0.1 mg/kg/day or higher damaged ovarian function in mice. SCCPs induced PANoptosis and oxidative stress, impacting female germline stem cells and hormone levels.
Area of Science:
- Environmental Toxicology
- Reproductive Toxicology
- Cellular Biology
Background:
- Short-chain chlorinated paraffins (SCCPs) are environmental contaminants with potential health risks.
- Limited research exists on the effects of low-level SCCP exposure on mammalian ovarian function.
- Understanding SCCP-induced reproductive toxicity is crucial for public health risk assessment.
Purpose of the Study:
- To investigate the impact of oral SCCP administration on ovarian damage in female mice.
- To determine the dose-response relationship between SCCP exposure and ovarian toxicity.
- To elucidate the cellular mechanisms underlying SCCP-induced ovarian dysfunction.
Main Methods:
- Female ICR mice were orally administered SCCPs at doses of 0, 0.01, 0.1, and 1.0 mg/kg/day for 21 days.
- Serum and ovarian tissues were collected for analysis.
- Ovarian follicle counts, oxidative stress markers, hormone levels (E2, anti-Müllerian hormone), PANoptosis, AIM2 and NLRP12 PANoptosome expression, and female germline stem cell (FGSC) markers were assessed.
Main Results:
- SCCPs at ≥0.1 mg/kg/day reduced ovarian follicle counts and induced dose-dependent oxidative stress.
- Serum E2 and ovarian anti-Müllerian hormone levels were decreased in SCCP-treated mice.
- SCCP exposure increased cellular PANoptosis in ovaries, elevated AIM2- and NLRP12-PANoptosome levels, and damaged FGSCs, diminishing their marker expression.
Conclusions:
- Oral administration of SCCPs at ≥0.1 mg/kg/day suppresses ovarian function in mice.
- SCCP-induced ovarian toxicity is associated with PANoptosis, oxidative stress, and damage to female germline stem cells.
- The findings suggest that SCCPs may pose a reproductive risk through the induction of AIM2- and NLRP12-PANoptosome in ovarian cells.
