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Effect of Proline on Cell Death, Cell Cycle, and Oxidative Stress in C6 Glioma Cell Line.

Authors
  • Ferreira, Andréa Gisiane Kurek1
  • Biasibetti-Brendler, Helena2
  • Sidegum, Daniele Susana Volkart2
  • Loureiro, Samanta Oliveira2
  • Figueiró, Fabrício3
  • Wyse, Angela T S2, 3
  • 1 Laboratório de Neuroproteção e Doenças Neurometabólicas, Departamento de Bioquímica, ICBS, UFRGS Rua Ramiro Barcelos, 2600-Anexo, Porto Alegre, RS, 90035-003, Brazil. [email protected] , (Brazil)
  • 2 Laboratório de Neuroproteção e Doenças Neurometabólicas, Departamento de Bioquímica, ICBS, UFRGS Rua Ramiro Barcelos, 2600-Anexo, Porto Alegre, RS, 90035-003, Brazil. , (Brazil)
  • 3 Departamento de Bioquímica, ICBS, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos, 2600-Anexo, Porto Alegre, RS, 90035-003, Brazil. , (Brazil)
Type
Published Article
Journal
Neurotoxicity Research
Publisher
Springer-Verlag
Publication Date
Nov 16, 2020
Identifiers
DOI: 10.1007/s12640-020-00311-z
PMID: 33196952
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Since proline metabolism has been implicated to play an underlying role in apoptotic signaling and cancer, and hyperprolinemic patients present susceptibility to tumors development, this study investigated the effect of proline on cell death, cell cycle, antioxidant enzymes activities, and immunocontent/activity of proteins involved in cell death/survival signaling pathways in C6 glioma cells. C6 cells were incubated with proline (0-5 mM) for 1 h, 24 h, 48 h, 72 h, or 7 days. Proline in high concentrations slightly decreased LDH release, and no cytotoxic effect was seen by Annexin-PI staining. Superoxide dismutase and catalase activities were increased by proline (1 mM) after 72 h, suggesting an increase in reactive species levels. Acetylcholinesterase activity was inhibited by proline at 1, 3, and 5 mM. The cell cycle progression was not altered. Results from Western blot analyses showed that proline at 1 mM after 72 h increased p-NF-ĸB and decreased acetylcholinesterase immunocontent but did not altered AKT, p-AKT, GSK3β, and p-GSK3β. Taken together, the data suggest that high proline levels seems to favor the signaling pathways towards cell proliferation, since acetylcholinesterase, which may act as tumor suppressor, is inhibited by proline. Also, p-NF-κB is increased by proline treatment and its activation is related to tumor cell proliferation and cellular response to oxidants. Proline also induced oxidative stress, but it appears to be insufficient to induce a significant change in cell cycle progression. These data may be related, at least in part, to the increased susceptibility to tumor development in hyperprolinemic individuals.

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