Related Experiment Video
Updated: May 10, 2026
Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease
Published on: January 7, 2014
Changes of MAO-A and MAO-B Expressions in the Placenta of MPTP or MPP(+) Treated Mice
Takafumi Sai1, Kazuyuki Uchida, Hiroyuki Nakayama
1Department of Veterinary Pathology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan ; Pathology Group, Toxicology and Pharmacokinetics Laboratories, Pharmaceutical Research Laboratories, Toray Industries, Inc., 6-10-1 Tebiro, Kamakura-shi, Kanagawa 248-8555, Japan.
Abstract:
In the present study, we evaluated the influence of intraperitoneal administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or 1-methyl-4-phenylpyridinium (MPP(+)) on the placenta. There was no increase in apoptotic cells in the placentas of C57BL/6 mice treated with 25.0 mg/kg MPTP or 17.1 mg/kg MPP(+), indicating that a single injection of the chemicals may induce very slight cytotoxicity in the placenta at 12 hr after administration. The decrease in the expression of monoamine oxidase (MAO)-A in the labyrinth zone and that of MAO-B in the basal zone may be due to the decrease in cell activity, whereas the increase of MAO-B expression in the labyrinth zone after MPTP treatment may be due to a responsive reaction caused by MPTP, one of the substrates of MAO-B. The results represent histological evidence that MAO-B may be involved in the metabolism of MPTP to MPP(+) in the labyrinth zone of the mouse placenta. In the present study, no increase in apoptotic cells indicates that MPTP and MPP(+) are hardly toxic to the placenta, and the histological change in MAO-B expression may indicate the possibility of involvement of placental MAO-B in MPTP metabolism.
Insights
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its metabolite 1-methyl-4-phenylpyridinium (MPP+) showed minimal placental toxicity in mice. Placental monoamine oxidase-B (MAO-B) may play a role in MPTP metabolism.
Area of Science:
- Toxicology
- Developmental Biology
- Neuroscience
Background:
- 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a neurotoxin known to induce Parkinsonism.
- The placenta plays a crucial role in fetal development and protection.
- The potential effects of MPTP and its metabolite MPP(+) on placental function are not well understood.
Purpose of the Study:
- To investigate the impact of MPTP and MPP(+) on mouse placental histology and cell apoptosis.
- To examine the expression of monoamine oxidase (MAO)-A and MAO-B in the placenta after MPTP/MPP(+) administration.
- To explore the potential role of placental MAO-B in MPTP metabolism.
Main Methods:
- C57BL/6 mice were administered single intraperitoneal injections of MPTP or MPP(+).
- Placental tissues were collected 12 hours post-administration for histological analysis.
- Apoptosis was assessed, and the expression of MAO-A and MAO-B was evaluated in different placental zones.
Main Results:
- No significant increase in apoptotic cells was observed in the placentas, suggesting low cytotoxicity.
- A decrease in MAO-A expression in the labyrinth zone and MAO-B in the basal zone was noted.
- MPTP treatment led to increased MAO-B expression in the labyrinth zone, indicating a responsive reaction.
Conclusions:
- MPTP and MPP(+) exhibit minimal toxicity to the mouse placenta at the tested doses.
- Histological changes in MAO-B expression suggest its potential involvement in the placental metabolism of MPTP to MPP(+).
- Further research is warranted to fully elucidate the placental handling of MPTP and its implications.
