Mitochondrial and Oxidative Stress Aspects in Hippocampus of Rats Submitted to Dietary n-3 Polyunsaturated Fatty Acid Deficiency After Exposure to Early Stress

Abstract

Chronic dietary long-chain polyunsaturated fatty acids (PUFAs) deficiency may lead to changes in cortex and hippocampus neuronal membrane phospholipids, and may be linked to impaired central nervous system function. Particularly docosahexaenoic acid deficiency appears to be involved in neuropsychiatric disorders. On the other hand, adverse events early in life may also profoundly affect brain development, leading to long-lasting effects on neurophysiology, neurobiology and behavior. This research assessed if neonatal stress and a dietary n-3 PUFAs deficiency could interact to produce hippocampal alterations related to mitochondrial functions in adult rats. There were no effects of diet, neonatal intervention or interactions on superoxide dismutase or catalase enzymatic activities, mitochondrial membrane potential and respiratory chain complexes. Rats fed n-3 PUFAs deficient diet displayed higher levels of glutathione peroxidase and catalase activity, higher free radicals production and higher thiol content compared to rats fed n-3 PUFAs adequate diet. There were interactions among diets and neonatal stress, since glutathione peroxidase, free radicals production and thiol content were increased in groups that were subjected to neonatal interventions fed n-3 PUFAs deficient diet. Additionally, reduced mitochondrial potential was observed in handled animals. Total thiol revealed a neonatal stress effect, since animals subjected to neonatal interventions displayed lower thiol content. In conclusion, we observed that a chronic treatment with deficient n-3 PUFAs diet, from the puberty period on, increased free radicals production and imbalanced antioxidant enzymes activities, and these increases were higher in animals subjected to neonatal interventions.

N‐3 PUFA‐Deficiency in Early Life Exhibits Aggravated MPTP‐Induced Neurotoxicity in Old Age while Supplementation with DHA/EPA‐Enriched Phospholipids Exerts a Neuroprotective Effect

“…[43] This study showed that n-3 PUFA-deficiency in the brain significantly aggravated the MPTP-induced oxidative stress and apoptosis degree, which was consistent with previous studies. [44] DHA/EPA-PLs consumption alleviated the damage by up-regulating the antioxidant enzyme levels and down-regulating the expressions of pro-apoptotic protein, but still did not recover to normal level in the n-3 PUFA-deficient mice.…”

The Mitochondrion as Potential Interface in Early-Life Stress Brain Programming

“…In an complementary approach, Ferreira et al (2015) studied the effects from the interaction between ELS and dietary deprivation of ω-3 PUFA on mitochondrial function and oxidative stress in rat hippocampus. Non-handled, handled or MS rat pups were fed postnatally until periadolescence (Table 1) diets either adequate or deficient in ω-3 PUFA.…”

“…Collectively, prenatal stress-dependent programing of offspring behavior and mitochondrial function can be normalized by a maternal DHA-rich diet. Relatedly, neonatal interventions can program altered susceptibility to oxidative stress (Ferreira et al, 2015) or overt oxidative dysregulation (Feng et al, 2012) in a manner dependent on the severity of the respective intervention. In any case, antioxidant treatments prevent behavioral and oxidative changes that arise from different qualities of stress exposure, whereby ω-3 PUFA is particularly effective against ELS reflecting its important role in early brain development.…”

Bioactive Compound Prodigiosin in Vivo Affecting the Nutrient Metabolism of Weaned Rats

“…These side effects lead to neuropsychiatric disorders, gastrointestinal dysfunction, and reduced immunity . Enhancing the digestion and absorption of nutrition is an effective strategy to alleviate adverse stresses arising from the environment and diet . After feeding, nutrient utilization directly affects the function of tested materials .…”