Effect of Dietary Protein Level and Origin on the Redox Status in the Digestive Tract of Mice

Abstract

Abstract:The present study was undertaken to evaluate the effects of high protein (soybean protein or casein) on the balance between production of free radicals and antioxidant level in digestive organs of mice. For this purpose, male (C57BL/6J) mice were adapted to experimental diets containing soybean protein or casein with 20% (normal protein diets, NPDs) or 60% (high protein diets, HPDs), and HPDs supplemented with 0.06g/kg cysteamine. After two weeks of feeding, oxidative and antioxidative parameters in duodenum, liver and pancreas were measured. The results show that ingestion of high protein markedly increased contents of superoxide anion and malondialdehyde (MDA), decreased activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and Na + K + -ATPase, and content of reduced glutathione (GSH) in digestive organs of mice (P<0.05). Levels of oxidative parameters were lower and antioxidant capacity of both enzyme and non-enzyme was higher in mice fed with soybean protein than those fed with casein. In groups fed HPDs supplemented with cysteamine, oxidative stress was mitigated. However, oxidative parameter levels were still higher than those of NPD-fed groups. The present study indicates that ingestion of high protein diets could result in an imbalance between oxidant and antioxidant, and thus induce oxidative stress in digestive organs of mice. The oxidative damage was smaller in mice fed with high level of soy protein in comparison with casein.

Effects of exposure to BDE-99 on oxidative status of liver and kidney in adult rats

“…The alteration in the activities of these enzymes, together with the alteration in the GSH-GSSG system, reflects that a single dose of BDE-99 can induce alterations in the oxidative system of the liver, even several weeks after exposure. It is known that when ROS generation overloads the antioxidants defense, the free radicals act on macromolecules such as proteins, lipids and nucleic acids, causing a chain reaction, in which intermediate species can act as oxidizing agents, altering the morphology and function cellular (Moreno et al, 2005;Gu et al, 2008).…”

Dietary protein affects urea transport across rat urothelia

“…In addition, we cannot rule out an independent bladder or urothelial factor(s), also dependent on dietary protein intake, possibly affecting urothelial urea reabsorption. Thus, if a high protein diet increases oxidative stress in bladder tissues as it does in digestive tissues (12), oxidative stress may influence urea transport in urothelial cells as it does in renal inner medullary collecting ducts where it has been shown to increase urea transport (49). Although such a bladder or urothelial factor is not apparent in an examination of the effect of dietary intake on numerical changes in concentration or quantity of urinary UN during bladder dwell, it must be considered given the small but significantly greater percentage of reabsorbed urea in the low and deficient dietary protein diet animal groups (26 and 23%) compared with the regular and high dietary protein groups (11 and 9%) as well as the greater percentage of reabsorbed UN in the low protein group (26%) compared with the 2% reabsorption in the high protein group of rats whose bladders were instilled with urine obtained during a previous low protein diet (LUHP group) and containing instilled concentration of UN similar to the low protein group.…”

Correlation between Oxidative Stress, Nutrition, and Cancer Initiation

“…Excessive protein consumption can induce amino acid oxidation and urea synthesis [ 210 ], and impair the nutritional efficacy of energy utilization [ 211 ]. An interesting study stated that high protein intake could obliterate the stability of antioxidants and oxidation of amino acids in the digestive system of mice and promote generation of ROS in the digestive gland [ 212 ]. A conceivable explanation is that ROS might be generated after meat consumption during its metabolism [ 213 ].…”