Abstract
Increased oxygen consumption and activation of specific metabolic pathways during or after physical exercise lead to the formation of reactive oxygen and nitrogen species. An investigation was made into the effects of pequi oil supplementation in protecting liver cells against injury resulting from oxidative stress. The experiments involved 20 male adult Wistar rats ( Rattus norvegicus). The animals were divided into four experimental groups: Group 1: sedentary control group; Group 2: exercise control group; Group 3: supplemented sedentary group; and Group 4: supplemented exercise group. Supplementation consisted of pequi oil administered by oral gavage (400 mg). The animals of the exercised groups were subjected to 20 swimming sessions for 5 weeks (with progressive increase of 10 minutes until exhaustion). Samples were collected from the right hepatic lobe for histopathological analysis and determination of malondialdehyde levels. The histopathological analyses revealed that the animals of the exercised control group had moderate liver damage, while the animals of the supplemented exercised group had slight tissue damage, and the sedentary control and sedentary supplemented groups showed no tissue damage. The malondialdehyde levels showed higher and statistically significant in exercise control group when compared to the other evaluated groups (p<0.05). In conclusion the supplementation with pequi oil had a protective effect on liver cells against damage caused by oxygen free radicals during strenuous exercise, as demonstrated by the indicator of lipid peroxidation.
Highlights
Increased oxygen consumption and activation of specific metabolic pathways during or after physical exercise lead to the formation of reactive oxygen and nitrogen species (RONS)
When the body undergoes periods of metabolic overload, such as that occurring during strenuous exercise, it accumulates reactive oxygen species (ROS) in the liver tissue, which can trigger tissue damage ranging from slight degeneration to cirrhosis
The animals were subjected to a natural photoperiod with water and feed ad libitum and were divided into four experimental groups with 5 animals: G1) sedentary control group; G2) exercise control group; G3) sedentary group supplemented with pequi oil; G4) exercise group supplemented with pequi oil
Summary
Increased oxygen consumption and activation of specific metabolic pathways during or after physical exercise lead to the formation of reactive oxygen and nitrogen species (RONS). It is known that physical exercising leads to the intense production of RONS arising from the activation of metabolic pathways such as increased mitochondrial activity (Fisher-Wellman and Bloomer, 2009; Miranda‐Vilela et al, 2016). When the body undergoes periods of metabolic overload, such as that occurring during strenuous exercise, it accumulates reactive oxygen species (ROS) in the liver tissue, which can trigger tissue damage ranging from slight degeneration to cirrhosis. In this regard, the liver is the organ most susceptible to the damaging effects of ROS, leading to numerous structural and functional injuries, which, despite its high regenerative capacity, can result in irreversible lesions (Araujo et al, 2013). One of the products generated by the breakdown of lipid chains is a substance known as malondialdehyde (MDA), and high levels of this substance indicate an increase in membrane lesions caused by ROS (Bezerra et al, 2004)
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