Cold stress on Araucaria angustifolia embryogenic cells results in oxidative stress and induces adaptation: implications for conservation and propagation

Abstract

Araucaria angustifolia (Bert.) O. Kuntze is a species critically endangered of extinction and its development and propagation is strongly affected by abiotic stress. We have previously shown the activation of uncoupling protein in A. angustifolia embryogenic stem cells subjected to cold stress. Now, we have furthered those studies by exposing these cells to cold stress (4 ± 1 °C for either 24 or 48 h) and evaluating parameters associated with oxidative stress and alterations in the cellular and mitochondrial responses. Cold stress affect the H₂O₂ levels and lipid peroxidation increased after both stress condition, an effect associated with the decrease in the activities of peroxidases, catalase and ascorbate/dehydroascorbate ratio. On the other hand, the activities of ascorbate peroxidase, monodehydroascorbate and dehydroascorbate reductases increased as an indication of adaptation. Another important impact of cold stress conditions was the decrease of external alternative NAD(P)H dehydrogenases activity and the increase of mitochondrial mass. These results show that cold stress induces oxidative stress in A. angustifolia embryogenic cells, which results in activation of the glutathione-ascorbate cycle as a compensation for the decrease in the activities of catalase, peroxidases, and external NAD(P)H dehydrogenases. Our results contribute to the understanding of the pathways that gymnosperms employ to overcome oxidative stress, which must be explored in order to improve the methods of conservation and propagation of A. angustifolia.

Keywords:

• Abiotic stress
• antioxidative response
• glutathione-ascorbate cycle
• NAD(P)H dehydrogenases alternatives
• somatic embryogenesis

Acknowledgements

The authors thank Dr. Ian Max Møller for your valuable comments and suggestions.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This investigation was supported by the Brazilian research funding agencies CNPq, CAPES, and INCT (Processos Redox em Biomedicina). Grant support was provided by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior – CAPES, FINEP (CT-Infra), Conselho Nacional de Desenvolvimento Científico e Tecnológico – CNPq (process 311629/2013-0), and INCT Redoxoma (process 573530/2008-4). The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.