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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Aluminum directly inhibits alternative oxidase pathway and changes metabolic and redox parameters on Jatropha curcas cell culture

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Author(s):
Vicentini, Tatiane M. [1] ; Cavalheiro, Amanda H. [1] ; Dechandt, Carlos R. P. [1] ; Alberici, Luciane C. [1] ; Vargas-Rechia, Carem G. [1]
Total Authors: 5
Affiliation:
[1] Univ Sao Paulo, Dept Chem & Phys, Sch Pharmaceut Sci Ribeirao Preto, Av Cafe S-N, BR-14040903 Ribeirao Preto, SP - Brazil
Total Affiliations: 1
Document type: Journal article
Source: Plant Physiology and Biochemistry; v. 136, p. 92-97, MAR 2019.
Web of Science Citations: 0
Abstract

Aluminum (Al) toxicity has been recognized to be a main limiting factor of crop productivity in acid soil. Al interacts with cell walls disrupting the functions of the plasma membrane and is associated with oxidative damage and mitochondrial dysfunction. Jatropha curcas L. (J. curcas) is a drought resistant plant, widely distributed around the world, with great economic and medicinal importance. Here we investigated the effects of Al on J. curcas mitochondrial function and cell viability, analyzing mitochondrial respiration, phenolic compounds, reducing sugars and cell viability in cultured J. curcas cells. The results showed that at 70 mu M, Al limited mitochondrial respiration by inhibiting the alternative oxidase (AOX) pathway in the respiratory chain. An increased concentration of reducing sugars and reduced concentration of intracellular phenolic compounds was observed during respiratory inhibition. After inhibition, a time-dependent upregulation of AOX mRNA was observed followed by restoration of respiratory activity and reducing sugar concentrations. Cultured J. curcas cells were very resistant to Al-induced cell death. In addition, at 70 mu M, Al also appeared as an inhibitor of cell wall invertase. In conclusion, Al tolerance in cultured J. curcas cells involves a inhibition of mitochondrial AOX pathway, which seems to start an oxidative burst to induce AOX upregulation, which in turn restores consumption of O-2 and substrates. These data provide new insight into the signaling cascades that modulate the Al tolerance mechanism. (AU)

FAPESP's process: 16/23509-4 - Identification of neuroprotective myokines released by human skeletal muscle at low and high intensity contractions: role of mitochondrial bioenergetics and oxidative stress
Grantee:Luciane Carla Alberici
Support Opportunities: Regular Research Grants