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The administration of food supplemented with cocoa powder during nutritional recovery reduces damage caused by oxidative stress in rat brain

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Abstract

Malnutrition contributes to the development of oxidative damage in the central nervous system. The selective administration of nutrients tends to show positive results in individuals who have suffered from malnutrition. To determine the effect of the administration of cocoa powder on the peroxidation of lipids and glutathione level during the nutritional recovery in brain, rats of 21 days old were subjected to a protocol that resembles malnutrition (MN) by feeding them with 60% of the daily food consumption of the control group (WN) and later to nutritional recovery with regular rodent feed (RFR) or added with cocoa (10 g of cocoa powder/kg of regular rodent feed) (CCR). Animals fed with regular rodent food showed significant reduction in brain glutathione: RFR (84.18 ± 6.38 ng/mg protein) vs. CCR (210.61 ± 50.10 ng/mg protein) and WN (186.55 ± 33.18 ng/mg protein), but with similar level to that of MN (92.12 ± 15.60 ng/mg protein). On the contrary, lipid peroxidation in RFR-fed animals increased RFR (1.32 ± 0.2 μM malondialdehyde/g of tissue), CCR (0.86 ± 0.07 μM malondialdehyde/g of tissue), WN (0.89 ± 0.09 μM malondialdehyde/g of tissue), but their thiobarbituric acid reactive substances concentration is similar to that of MN group (1.50 ± 0.2 μM malondialdehyde/g of tissue). Consumption of cocoa powder as a source of antioxidants favors the restoration of the concentration of glutathione and reduces the damage caused by oxidative stress during nutritional recovery in rat brain.

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Acknowledgments

The authors want to express their gratitude to Dr. Cyril Ndidi Nwoye, a native English speaker, for translating this manuscript.

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We declared that there are no conflicts of interest.

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Correspondence to Hugo Juárez Olguín.

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Barragán Mejía, G., Calderón Guzmán, D., Juárez Olguín, H. et al. The administration of food supplemented with cocoa powder during nutritional recovery reduces damage caused by oxidative stress in rat brain. Naunyn-Schmiedeberg's Arch Pharmacol 384, 499–504 (2011). https://doi.org/10.1007/s00210-011-0676-0

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