Literature DB >> 36214987

Autophagy in Neurons of the Prefrontal Cortex and Hippocampus of Rats after Trimethyltin Chloride Intoxication.

I B Mikheeva1, E V Pershina2, I Yu Chernomorets2, N S Zhuikova2, L L Pavlik2, V I Arkhipov2.   

Abstract

Ultrastructural studies of the hippocampus and the prefrontal cortex of rats were performed 7, 30, and 50 days after their damage by neurotoxicant trimethyltin chloride (TMT). Significant damage to neurons was observed in both brain structures. In the hippocampus, a large number of autophagosomes (0.9±0.1 per μm2) appeared in the soma of neurons, dendrites, and axons in 7 days after intoxication. In addition, we observed the appearance of hyperchromic neurons with abnormal structure of mitochondria. In the prefrontal cortex, damaged neurons also contained autophagosomes, but their number was significantly lower (0.3±0.1 per μm2). The number of autophagosomes decreased with increasing the time after TMT administration: 30 days after injection, the content of autophagosomes in the hippocampus was 0.10±0.01 per μm2, while in the prefrontal cortex, autophagosomes were no longer found. We hypothesized that autophagy in the hippocampus was not effective enough to prevent neuronal death caused by the neurotoxicant.
© 2022. Springer Science+Business Media, LLC, part of Springer Nature.

Entities:  

Keywords:  autophagosomes; hippocampus; mitochondria; prefrontal cortex; trimethyltin chloride

Mesh:

Substances:

Year:  2022        PMID: 36214987     DOI: 10.1007/s10517-022-05608-x

Source DB:  PubMed          Journal:  Bull Exp Biol Med        ISSN: 0007-4888            Impact factor:   0.737


  10 in total

1.  Expression of mGlu Receptor Genes in the Hippocampus After Intoxication with Trimethyltin.

Authors:  E V Pershina; I B Mikheeva; E R Kamaltdinova; V I Arkhipov
Journal:  J Mol Neurosci       Date:  2018-11-30       Impact factor: 3.444

Review 2.  Life and death partners: apoptosis, autophagy and the cross-talk between them.

Authors:  A Eisenberg-Lerner; S Bialik; H-U Simon; A Kimchi
Journal:  Cell Death Differ       Date:  2009-03-27       Impact factor: 15.828

3.  Quantitative mapping of trimethyltin injury in the rat brain using magnetic resonance histology.

Authors:  G Allan Johnson; Evan Calabrese; Peter B Little; Laurence Hedlund; Yi Qi; Alexandra Badea
Journal:  Neurotoxicology       Date:  2014-03-11       Impact factor: 4.294

Review 4.  Autophagy in trimethyltin-induced neurodegeneration.

Authors:  Elena Pompili; Cinzia Fabrizi; Lorenzo Fumagalli; Francesco Fornai
Journal:  J Neural Transm (Vienna)       Date:  2020-05-25       Impact factor: 3.575

Review 5.  Trimethyltin-induced hippocampal degeneration as a tool to investigate neurodegenerative processes.

Authors:  Maria Concetta Geloso; Valentina Corvino; Fabrizio Michetti
Journal:  Neurochem Int       Date:  2011-03-22       Impact factor: 3.921

Review 6.  Functional and structural properties of stannin: roles in cellular growth, selective toxicity, and mitochondrial responses to injury.

Authors:  M L Billingsley; J Yun; B E Reese; C E Davidson; B A Buck-Koehntop; G Veglia
Journal:  J Cell Biochem       Date:  2006-05-15       Impact factor: 4.429

Review 7.  Trimethyltin-induced hippocampal neurodegeneration: A mechanism-based review.

Authors:  Sueun Lee; Miyoung Yang; Jinwook Kim; Sohi Kang; Juhwan Kim; Jong-Choon Kim; Chaeyong Jung; Taekyun Shin; Sung-Ho Kim; Changjong Moon
Journal:  Brain Res Bull       Date:  2016-07-20       Impact factor: 4.077

8.  Mitochondrial oxygen consumption inhibition importance for TMT-dependent cell death in undifferentiated PC12 cells.

Authors:  Francesco Misiti; Federica Orsini; M Elisabetta Clementi; Wanda Lattanzi; Bruno Giardina; Fabrizio Michetti
Journal:  Neurochem Int       Date:  2007-12-04       Impact factor: 3.921

Review 9.  Methylated tin toxicity a reappraisal using rodents models.

Authors:  A Trabucco; P Di Pietro; S L Nori; F Fulceri; L Fumagalli; A Paparelli; F Fornai
Journal:  Arch Ital Biol       Date:  2009-12       Impact factor: 1.000

  10 in total

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