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A Murine Pancreatic Islet Cell-based Screening for Diabetogenic Environmental Chemicals
Published on: June 25, 2018
Leping Ye1, Jingjing Guo1, Ren-Shan Ge1
1The 2nd Affiliated Hospital and Research Academy of Reproductive Biomedicine of Wenzhou Medical University, Wenzhou, Zhejiang, PR China.
This review explores how environmental pollutants may interfere with hydroxysteroid dehydrogenases (HSDs), enzymes that regulate steroid hormone levels. The study identifies industrial chemicals, pesticides, and plant compounds that inhibit specific HSDs. These pollutants include perfluoroalkyl compounds, phthalates, and organotins. The findings suggest that such chemicals may disrupt hormone metabolism. The authors propose that exposure to these pollutants could affect endocrine function. They highlight the need for further research on the effects of these chemicals. The study compiles evidence from multiple sources to inform future investigations.
Area of Science:
Background:
Current understanding of hydroxysteroid dehydrogenases (HSDs) shows they are key in steroid hormone metabolism. Four HSD classes are known to regulate steroid interconversions. 3β-HSDs convert pregnenolone and related steroids into active forms. 11β-HSDs manage cortisol and cortisone levels. 17β-HSDs handle androgen and estrogen conversions. 20α-HSDs act on progesterone derivatives. Prior research has shown these enzymes are critical for hormone balance. No prior work had resolved how environmental chemicals might affect them. This gap motivated a review of known inhibitors. The study aimed to clarify which pollutants interfere with HSD activity.
Purpose Of The Study:
This review aimed to identify environmental pollutants that inhibit hydroxysteroid dehydrogenases. The authors focused on how these chemicals affect steroid hormone levels. They examined industrial compounds, pesticides, and plant constituents. The goal was to compile evidence on HSD inhibition by environmental agents. They sought to highlight which pollutants are most commonly linked to enzyme disruption. The study also aimed to summarize the mechanisms of inhibition. It proposed that such pollutants may disrupt endocrine function. The review sought to inform further research on chemical exposure effects.
Main Methods:
The authors conducted a literature review of known hydroxysteroid dehydrogenase inhibitors. They categorized pollutants into industrial, pesticide, and plant-derived groups. They analyzed each chemical’s reported effects on HSD activity. The study focused on four HSD classes: 3β-, 11β-, 17β-, and 20α-HSDs. They summarized findings from prior experimental studies. The review included perfluoroalkyl compounds, phthalates, and bisphenol A. They also examined methoxychlor, organotins, and genistein. The approach involved synthesizing evidence from multiple sources.
Main Results:
The study found that perfluoroalkyl compounds inhibit 3β-HSD activity. Phthalates and bisphenol A were linked to 11β-HSD inhibition. Organotins and methoxychlor were shown to affect 17β-HSDs. Benzophenone and prochloraz were also identified as inhibitors. 20α-HSDs were affected by 1,2-dibromo-3-chloropropane. Plant-derived compounds like genistein and gossypol were included. The review highlighted that these pollutants may disrupt steroid hormone levels. The findings suggest a need for further study on exposure effects.
Conclusions:
The authors concluded that environmental pollutants may inhibit hydroxysteroid dehydrogenases. They proposed that such inhibition could disrupt steroid hormone metabolism. The review suggests that perfluoroalkyl compounds and phthalates are significant inhibitors. They noted that organotins and methoxychlor also interfere with HSD activity. The study emphasized the need for more research on pollutant effects. They suggested that these chemicals may contribute to endocrine disruption. The authors highlighted the importance of monitoring exposure levels. They proposed that future studies should explore mechanisms of inhibition.
Environmental pollutants may inhibit HSD enzymes, disrupting steroid hormone metabolism.
Phthalates, bisphenol A, and benzophenone are associated with 11β-HSD inhibition.
11β-HSDs convert cortisol to cortisone, regulating active hormone levels in the body.
Genistein, gossypol, and licorice compounds may inhibit specific HSD enzymes.
Perfluoroalkyl compounds may inhibit 3β-HSD, altering steroid biosynthesis.
The authors suggest pollutants may disrupt steroid hormone metabolism through HSD inhibition.