Publication: Almond skin extracts and chlorogenic acid delay chronological aging and enhanced oxidative stress response in yeast
Issued Date
2020-06-01
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20751729
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2-s2.0-85085622585
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Mahidol University
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SCOPUS
Bibliographic Citation
Life. Vol.10, No.6 (2020)
Suggested Citation
Duangjai Tungmunnithum, Malika Abid, Ahmed Elamrani, Samantha Drouet, Mohamed Addi, Christophe Hano Almond skin extracts and chlorogenic acid delay chronological aging and enhanced oxidative stress response in yeast. Life. Vol.10, No.6 (2020). doi:10.3390/life10060080 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/57605
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Title
Almond skin extracts and chlorogenic acid delay chronological aging and enhanced oxidative stress response in yeast
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Abstract
© 2020 by the authors. Licensee MDPI, Basel, Switzerland. Almond (Prunus dulcis (Mill.) D.A.Webb) is one of the largest nut crops in the world. Recently, phenolic compounds, mostly stored in almond skin, have been associated with much of the health-promoting behavior associated with their intake. The almond skin enriched fraction obtained from cold-pressed oil residues of the endemic Moroccan Beldi ecotypes is particularly rich in chlorogenic acid. In this study, both almond skin extract (AE) and chlorogenic acid (CHL) supplements, similar to traditional positive control resveratrol, significantly increased the chronological life-span of yeast compared to the untreated group. Our results showed that AE and CHL significantly reduced the production of reactive oxygen and nitrogen species (ROS/RNS), most likely due to their ability to maintain mitochondrial function during aging, as indicated by the maintenance of normal mitochondrial membrane potential in treated groups. This may be associated with the observed activation of the anti-oxidative stress response in treated yeast, which results in activation at both gene expression and enzymatic activity levels for SOD2 and SIR2, the latter being an upstream inducer of SOD2 expression. Interestingly, the differential gene expression induction of mitochondrial SOD2 gene at the expense of the cytosolic SOD1 gene confirms the key role of mitochondrial function in this regulation. Furthermore, AE and CHL have contributed to the survival of yeast under UV-C-induced oxidative stress, by reducing the development of ROS/RNS, resulting in a significant reduction in cellular oxidative damage, as evidenced by decreased membrane lipid peroxidation, protein carbonyl content and 8-oxo-guanine formation in DNA. Together, these results demonstrate the interest of AE and CHL as new regulators in the chronological life-span and control of the oxidative stress response of yeast.