High Protein Diet Induces Oxidative Stress in Rat Cerebral Cortex and Hypothalamus

Int J Mol Sci. 2019 Mar 28;20(7):1547. doi: 10.3390/ijms20071547.

Abstract

This is the first study to analyze the impact of high protein diet (HPD) on antioxidant defense, redox status, as well as oxidative damage on both a local and systemic level. Male Wistar rats were divided into two equal groups (n = 9): HPD (44% protein) and standard diet (CON; 24.2% protein). After eight weeks, glutathione peroxidase (GPx), glutathione reductase (GR), catalase (CAT), superoxide dismutase-1 (SOD-1), reduced glutathione (GSH), uric acid (UA), total antioxidant (TAC)/oxidant status (TOS) as well as advanced glycation end products (AGE), 4-hydroxynonenal (4-HNE), and malondialdehyde (MDA) were analyzed in the serum/plasma, cerebral cortex, and hypothalamus of HPD and CON rats. HPD resulted in higher UA concentration and activity of GPx and CAT in the hypothalamus, whereas in the cerebral cortex these parameters remained unchanged. A significantly lower GSH content was demonstrated in the plasma and hypothalamus of HPD rats when compared to CON rats. Both brain structures expressed higher content of 4-HNE and MDA, whereas AGE was increased only in the hypothalamus of HPD animals. Despite the enhancement in antioxidant defense in the hypothalamus, this mechanism does not protect the hypothalamus from oxidative damage in rats. Hypothalamus is more susceptible to oxidative stress caused by HPD.

Keywords: cerebral cortex; high protein diet; hypothalamus; oxidative damage; oxidative stress.

MeSH terms

  • Animals
  • Catalase / analysis
  • Catalase / metabolism
  • Cerebral Cortex / metabolism*
  • Cerebral Cortex / pathology
  • Diet, High-Protein / adverse effects*
  • Glutathione Peroxidase / analysis
  • Glutathione Peroxidase / metabolism
  • Glutathione Reductase / analysis
  • Glutathione Reductase / metabolism
  • Glycation End Products, Advanced / analysis
  • Glycation End Products, Advanced / metabolism
  • Hypothalamus / metabolism*
  • Hypothalamus / pathology
  • Male
  • Malondialdehyde / analysis
  • Malondialdehyde / metabolism
  • Oxidative Stress*
  • Rats, Wistar

Substances

  • Glycation End Products, Advanced
  • Malondialdehyde
  • Catalase
  • Glutathione Peroxidase
  • Glutathione Reductase