This study investigated the suppressive eff ects of Armoracia rusticana (AR) and its three main glucosinolates on both free and bound heterocyclic amines (HAs), along with their mechanisms of free radical quenching using density functional theory. Fish patties were supplemented with varying concentrations of AR (0.5%‒1.5%) and glucosinolates (0.005%‒0.015%), showing a dose-dependent inhibition of HAs and concurrent elimination of free radicals and HAs intermediates. Glucobrassicin demonstrated the highest reactivity, which was verified by frontier orbit analysis and conceptual density functional parameters, consistent with experimental findings. Furthermore, the O-H bond connected to the sulfur atom of glucobrassicin possessed the smallest bond dissociation enthalpy (BDE) value, which indicated that this particular hydrogen atom is most susceptible to react with free radicals. Overall, AR and its glucosinolates, especially glucobrassicin, show promise as natural additives for improving food safety and quality.
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Open Access
Research Article
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Open Access
Issue
To investigate the effect of dietary acrylamide exposure on the progression of type 2 diabetes in GK rats.
The effects of intragastric administration of acrylamide (2 mg/(kg mb·d)) for eight weeks on blood glucose metabolism indicators in GK rats including fasting blood glucose, fasting glucose tolerance and insulin sensitivity were evaluated. Meanwhile, the levels of serum biochemical indexes, oxidative stress and inflammatory factors were determined, and pathological changes of the liver, kidney, pancreas and gastrocnemius muscle were observed by hematoxylin-eosin (HE) staining to examine the effect of acrylamide exposure on organ functions of GK rats. In addition, serum and urine metabolites were detected by gas chromatography-mass spectrometry (GC-MS), the major differential metabolites between the acrylamide exposure and control (deionized water) groups were identified and related metabolic pathways were analyzed.
Compared with the control group, dietary acrylamide exposure further damaged the pancreas of GK rats, promoted oxidative stress and inflammatory factors, and affected islet β-cell function and the pentose phosphate metabolic pathway, aggravating blood glucose metabolism disorder, as manifested by a significant increase in fasting blood glucose levels (P < 0.05), impaired fasting glucose tolerance and decreased insulin sensitivity. In addition, the differential metabolites identified included L-tyrosine, inositol, hippuric acid, citraconic acid, phenylacetylglycine, N-acetylleucine, quinolinic acid, L-tryptophan and 5-hydroxymethyltryptamine, which were associated with the metabolic pathways of amino acids such as arginine, proline, tryptophan, phosphoinositide, phenylalanine, tyrosine and tryptophan. These metabolites and metabolic pathways are thought to be associated with abnormal liver and neural tissue functions. Serum biochemical and pathological analysis confirmed that dietary acrylamide exposure could cause different degrees of damage to the liver, gastrocnemius muscle and nerve tissue of GK rats.
Dietary acrylamide exposure has serious adverse effects on the health of diabetic GK rats, aggravating blood glucose metabolism disorder and affecting the function of organs and tissues.
Open Access
Research Article
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Diabetes-associated cognitive dysfunction has already been attracted considerable attention. Advanced glycation end products (AGEs) from daily diets are thought to be a vital contributor to the development of this diseases. However, the effect of one of the best-characterized exogenous AGEs Nε-(carboxymethyl)lysine (CML) on cognitive function is not fully reported. In the present study, diabetical Goto-Kakizaki (GK) rats were treated with free CML for 8-weeks. It was found that oral consumption of exogenous CML significantly aggravated diabetes-associated cognitive dysfunction in behavioral test. In details, exogenous CML increased levels of oxidative stress, promoted the activation of glial cells in the brain, up-regulated the release of inflammatory cytokines interleukin-6, inhibited the protein expression of the brain-derived neurotrophic factor and thus led to neuroinflammation. Furthermore, exogenous CML promoted the amyloidogenesis in the brain of GK rats, and inhibited the expression of GLUT4. Additionally, several tricarboxylic acid cycle and glutamate-glutamine/γ-aminobutyric acid cycle intermediates including pyruvate, succinic acid, glutamine, glutamate were significantly changed in brain of GK rats treated with exogenous free CML. In conclusion, exogenous free CML is a potentially noxious compounds led to aggravated diabetes-associated cognitive dysfunction which could be possibly explained by its effects on neuroinflammation, energy and neurotransmitter amino acid homeostasis.
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