Investigation of the effects of acrylamide applied during pregnancy on fetal brain development in rats and protective role of the vitamin E

Abstract

<jats:p> A liberal amount of acrylamide (AA) is produced as a result of frying or baking foods in high temperatures, and individuals take certain amounts of AA everyday by consuming these food items. Pregnant women are also exposed to AA originating from food during pregnancy and their fetus are probably affected. The rats were divided into five different groups: control (C), corn oil (CO), vitamin E (Vit E), AA, and Vit E + AA, with eight pregnant rats in each group. On the 20th day of pregnancy, fetuses were removed and brain tissues of fetuses were examined for biochemical and histological changes. AA caused degeneration in neuron structures in fetal brain tissue and caused hemorrhagic damages; dramatically decreased brain-derived neurotrophic factor levels; increased malondialdehyde, total oxidant capacity levels; and decreased reduced glutathione and total antioxidant capacity levels ( p &lt; 0.05). On the other hand, it was determined that the Vit E, a neuroprotectant and a powerful antioxidant, suppressed the effects of AA on fetal development and fetal brain tissue damage for the above-mentioned parameters ( p &lt; 0.05). It is recommended to consume food containing Vit E as a protection to minimize the toxic effects of food-oriented AA on fetus development due to the widespread nature of fast-food culture in today’s life and the impossibility of protection from AA toxicity. </jats:p>

Minocycline protects against acrylamide-induced neurotoxicity and testicular damage in Sprague-Dawley rats

“…In our study, treatment of rats with ACR increased MDA concentrations in both brain and testicular tissues compared to vehicle-treated rats. Consistent with our study, it was reported previously that treatment of rats with ACR significantly increases MDA levels in the nervous system 43,44,45 and the testes 36,46 . Treatment with MIN significantly decreased MDA concentrations in the brain and testicular tissues of ACR-treated rats indicating its antioxidant effects.…”

Protective effect of carnosic acid on acrylamide‐induced liver toxicity in rats: Mechanistic approach over Nrf2‐Keap1 pathway

“…In our study, the lowest CAT and TAC levels and highest MDA, TOS, and OSI levels were in the AA group, which shows that acrylamide decreases cellular antioxidant stores, increases oxidative radicals, thereby triggering oxidative stress. Erdemli et al [ 27 ] reported that acrylamide‐induced TAC decreases, and MDA and TOS increase in their study over fetal brain development during pregnancy. In addition, in the study of Chen et al, [ 28 ] acrylamide led to oxidative damage by producing oxygen radicals and reducing the enzymatic antioxidants of CAT and SOD.…”

α-Tocopherol and Hippocampal Neural Plasticity in Physiological and Pathological Conditions

“…High maternal intake of vitamin E was shown to protect offspring development in rodent experimental pregnancy models, i.e., decreasing embryo malformations in gestational diabetes [43,44,45,46,47], and reducing brain atrophy and DNA damage in ethanol-exposed mothers [48], suppressing neuronal degeneration and hemorrhagic damage in fetal brain exposed in utero to neurotoxicants, such as acrylamide [49]. Despite encouraging preclinical evidence, clinical trials found no clear association in humans between maternal vitamin E supplementation and the rate of fetal malformations, preterm birth, and neonatal or perinatal death [50,51,52,53,54].…”

“…Distinct PKC isozymes [68] are differentially expressed in neural tissues, where they function as signal transducers in a variety of brain developmental processes, such as cell proliferation and differentiation, dendritic growth, synapse formation and pruning [69,70,71,72,73,74,75]. It is worth noting that alterations of PKC isozymes’ activity and/or expression are involved in brain developmental dysfunctions associated with neurotoxicant exposure occurring during gestational and perinatal periods [49,76,77]. Based on this rationale, we tested the hypothesis that maternal supranutritional intake of α-T could affect PKC function in fetal and early postnatal brain, thereby influencing neurodevelopmental processes in the progeny [78,79,80].…”