Impact of Maternal Folic Acid Supplementation on Descendants' Kidney in Adulthood.

Unlabelled: Supplementation with folic acid (FA) during gestation has been recommended by medical society all over the world, but some studies have shown that intake of high folic acid diet may unleash damages to the descendants.

Objectives: Describing the effects of maternal supplementation with FA during gestation on offspring's kidney at late life stages.

Data Source: It is a systematic review by which were consulted the following databases: Medline, through Pubmed, Lilacs, and SciELO.

A Pretreatment with Isoorientin Attenuates Redox Disruption, Mitochondrial Impairment, and Inflammation Caused by Chlorpyrifos in a Dopaminergic Cell Line: Involvement of the Nrf2/HO-1 Axis.

The C-glucosyl flavone isoorientin (ISO) is obtained by humans from the diet and exhibits several cytoprotective effects, as demonstrated in different experimental models. However, it was not previously shown whether ISO would be able to prevent mitochondrial impairment in cells exposed to a chemical stressor. Thus, we treated the human neuroblastoma SH-SY5Y cells with ISO (0.

The isothiocyanate sulforaphane prevents mitochondrial impairment and neuroinflammation in the human dopaminergic SH-SY5Y and in the mouse microglial BV2 cells: role for heme oxygenase-1.

Sulforaphane (SFN) promotes protective effects in different cell types. Nonetheless, it remains to be clarified by which mechanism SFN exerts benefits in mammalian cells. Mitochondria are a major source of adenosine triphosphate (ATP) and reactive species in nucleated cells.

The C-glucosyl flavone isoorientin pretreatment attenuates the methylglyoxal-induced mitochondrial dysfunction in the human neuroblastoma SH-SY5Y cells: role for the AMPK-PI3K/Akt/Nrf2/γ-GCL/GSH axis.

The reactive dicarbonyl methylglyoxal (MG) behaves as a pro-oxidant agent, causing redox dysfunction and cell death by different mechanisms in mammalian cells. MG is also a mitochondrial toxicant, impairing the oxidative phosphorylation (OXPHOS) system and leading to bioenergetics and redox collapses. MG induces glycation and exerts an important role in neurodegenerative and cardiovascular diseases.

Suppression of Mitochondria-Related Bioenergetics Collapse and Redox Impairment by Tanshinone I, a Diterpenoid Found in Salvia miltiorrhiza Bunge (Danshen), in the Human Dopaminergic SH-SY5Y Cell Line Exposed to Chlorpyrifos.

Tanshinone I (T-I, CHO) is a diterpene found in Salvia miltiorrhiza Bunge (Danshen) and promotes cytoprotection in several experimental models. Chlorpyrifos (CPF) is an agrochemical that causes bioenergetics failure, redox impairment, inflammation, and cell death in animal tissues. Here, we investigated whether T-I would be able to prevent the consequences resulting from the exposure of the human dopaminergic SH-SY5Y cells to CPF.

Pinocembrin pretreatment counteracts the chlorpyrifos-induced HO-1 downregulation, mitochondrial dysfunction, and inflammation in the SH-SY5Y cells.

Chlorpyrifos (CPF), an insecticide, induces pro-oxidant, pro-inflammatory, and pro-apoptotic effects in animal cells. Contamination with CPF occurs not only in farms, since CPF is found in the food consumed in homes. Recently, it was demonstrated that CPF affects the mitochondria, inhibiting components of the electron transfer chain (ETC), causing loss of mitochondrial membrane potential (MMP), and reducing the synthesis of adenosine triphosphate (ATP) by the Complex V.

Astaxanthin prevents mitochondrial impairment in the dopaminergic SH-SY5Y cell line exposed to glutamate-mediated excitotoxicity: Role for the Nrf2/HO-1/CO-BR axis.

Mitochondrial dysfunction has been viewed in several diseases, including neurological disorders. In the glutamate (GLU)-mediated excitotoxicity, it has been described mitochondrial impairment, disrupted redox environment, and increased rates of cell death in the affected brain areas. Astaxanthin (AST) is a potent antioxidant and anti-inflammatory xanthophyll that also promotes beneficial mitochondria-related effects in brain cells.

Effects of nandrolone decanoate on femur morphology. Experimental study.

Purpose: To evaluate the immediate and late effects of nandrolone on femur morphology of rats.

Methods: Twenty-eight animals with 20 weeks of age were divided into four groups: C28, control animals that were euthanized eight weeks after the experiment started; C40, control animals euthanized 20 weeks after the experiment started; T28, treated animals receiving nandrolone during eight weeks and euthanized immediately after the treatment period; and T40, animals treated during eight weeks and euthanized 12 weeks after the end of the treatment. Treated animals received nandrolone decanoate during eight weeks and control groups received peanut oil by intramuscular injection.

The signaling pathway PI3K/Akt/Nrf2/HO-1 plays a role in the mitochondrial protection promoted by astaxanthin in the SH-SY5Y cells exposed to hydrogen peroxide.

The mitochondria are the major source of reactive species in the mammalian cells. Hydrogen peroxide (HO) is a potent inducer of redox impairment by a mechanism, at least in part, dependent on its ability to impair mitochondrial function. HO plays an important role in several pathological conditions, including neurodegeneration and cardiovascular diseases.

The Isothiocyanate Sulforaphane Depends on the Nrf2/γ-GCL/GSH Axis to Prevent Mitochondrial Dysfunction in Cells Exposed to Methylglyoxal.

Methylglyoxal (MG) is a reactive dicarbonyl presenting both endogenous (e.g. glycolysis) and exogenous (e.

Mitochondrial Protection and Anti-inflammatory Effects Induced by Emodin in the Human Neuroblastoma SH-SY5Y Cells Exposed to Hydrogen Peroxide: Involvement of the AMPK/Nrf2 Signaling Pathway.

Emodin (EM; 1,3,8-trihydroxy-6-methylanthracene-9,10-dione; CHO) is an anthraquinone and exerts cytoprotective effects, as observed in both in vitro and in vivo experimental models. Mitochondrial dysfunction induced by reactive species plays a central role in the onset and progression of different human diseases. Thus, we have tested here whether a pretreatment (for 4 h) with EM (at 40 µM) would be able to promote mitochondrial protection in the human neuroblastoma SH-SY5Y cells exposed to the pro-oxidant agent hydrogen peroxide (HO).

Promotion of Mitochondrial Protection by Emodin in Methylglyoxal-Treated Human Neuroblastoma SH-SY5Y Cells: Involvement of the AMPK/Nrf2/HO-1 Axis.

Mitochondrial dysfunction is part of the mechanism of several human diseases. This negative circumstance may be induced by certain toxicants, as methylglyoxal (MG). MG is a reactive dicarbonyl presenting both endogenous and exogenous sources and is also able to induce protein cross-linking and glycation.

Nrf2 Mediates the Anti-apoptotic and Anti-inflammatory Effects Induced by Gastrodin in Hydrogen Peroxide-Treated SH-SY5Y Cells.

Redox impairment, inflammation, and increased rates of cell death are central players during neurodegeneration. In that context, activation of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) has been viewed as an interesting strategy in order to reduce the impact of redox dysfunction and neuroinflammation on cell fate. There is evidence indicating that the benefits caused by natural products in the brain may be due to the ability of these agents in upregulating Nrf2.

Sulforaphane Attenuated the Pro-Inflammatory State Induced by Hydrogen Peroxide in SH-SY5Y Cells Through the Nrf2/HO-1 Signaling Pathway.

Sulforaphane (SFN), an isothiocyanate obtained from cruciferous vegetables, exerts antioxidant, antiapoptotic, and antitumor activities in different cell types. Moreover, SFN has been viewed as an anti-inflammatory agent. Nonetheless, the mechanism underlying the ability of SFN in modulating the immune response in mammalian cells is not completely understood yet.

Naringenin Attenuates HO-Induced Mitochondrial Dysfunction by an Nrf2-Dependent Mechanism in SH-SY5Y Cells.

Mitochondria are the major site of ATP production in mammalian cells. Furthermore, these organelles are a source and a target of reactive oxygen species (ROS), such as radical anion superoxide (O) and hydrogen peroxide (HO). The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is the master regulator of the mammalian redox biology and controls the expression of antioxidant and phase II detoxifying enzymes in several cell types.

Pinocembrin Suppresses HO-Induced Mitochondrial Dysfunction by a Mechanism Dependent on the Nrf2/HO-1 Axis in SH-SY5Y Cells.

Mitochondria are susceptible to redox impairment, which has been associated with neurodegeneration. These organelles are both a source and target of reactive species. In that context, there is increasing interest in finding natural compounds that modulate mitochondrial function and mitochondria-related signaling in order to prevent or to treat diseases involving mitochondrial impairment.

The impact of dietary organic and transgenic soy on the reproductive system of female adult rat.

The goal of this article was to compare the effects of a prolonged use of organic and transgenic soy on the lipid profile and ovary and uterus morphology. Wistar rats were fed three different diets from weaning until sacrifice at 15 months of age. The three diets were: casein-based diet control group (CG), organic soy-based diet group (OSG), or transgenic soy-based diet group (GMSG).

Maternal malnutrition during lactation alters the folliculogenesis and gonadotropins and estrogen isoforms ovarian receptors in the offspring at puberty.

In this study, we aimed to evaluate whether maternal malnutrition during lactation alters the folliculogenesis and the expression of the gonadotropins and estrogen isoforms ovarian receptors in the offspring at puberty. At parturition, dams were randomly assigned to the following groups: control (C) group, with free access to a standard laboratory diet containing 23% protein and protein-energy-restricted (PER) group, with free access to an isoenergy and protein-restricted diet containing 8% protein. After weaning, the female pups had free access to standard laboratory diet.

[Assessing autonomic function in hypertrophic cardiomyopathy].

Objective: Assess the autonomic function in hypertrophic cardiomyopathy (HCM) through heart rate variability (HRV) and to correlate it to echocardiographic data.

Methods: Two groups were studied, and compared for gender, age and HR: A) Ten (10) patients reporting septal HCM (70% non-obstructive); B) Ten (10) healthy volunteers. HRV was analyzed along four successive stages: at rest, under controlled breathing, while bending, and controlled breathing associated to bending.

The pups' endometrium morphology is affected by maternal malnutrition during suckling.

Objectives: This study aims to determine the effects of maternal protein and energy malnutrition during lactation on the endometrial structures of the offspring at puberty.

Methods: At parturition, dams were randomly assigned to the following groups: control group (C), with free access to a standard laboratory diet containing 23% protein; protein-restricted (PR) group, with free access to an isoenergy and protein-restricted diet containing 8% protein; and energy-restricted (ER) group, receiving standard laboratory diet in restricted quantities. After weaning, all female pups had free access to standard laboratory diet.

Detection of incipient left ventricular hypertrophy in mild to moderate arterial hypertension with normal electrocardiogram and echocardiogram: a new use for signal-averaged electrocardiography.

Objective: To assess signal-averaged electrocardiogram (SAECG) for diagnosing incipient left ventricular hypertrophy (LVH).

Methods: A study with 115 individuals was carried out. The individuals were divided as follows: GI - 38 healthy individuals; GII - 47 individuals with mild to moderate hypertension and normal findings on echocardiogram and ECG; and GIII - 30 individuals with hypertension and documented LVH.