Six hydroxycinnamic acids were identified and determined quantitatively in methanol and acetone extracts from quince peel and pulp, namely 3-O-caffeoylquinic acid (3-CQA), 4-p-coumaroylquinic acid (HC1), 4-O-caffeoylquinic acid (4-CQA), 5-O-caffeoylquinic acid (5-CQA), derivative of p-coumaroylquinic acid (HC2) and 3,5-dicaffeoylquinic acid (3,5-diCQA). The most abundant hydroxycinnamic acid was 5-CQA (neochlorogenic acid) with 259.12-481.4mg/kgf.w. in peel and 97.33-217.36mg/kg in quince pulp. Six flavonols were determined in the extracts from quince, quercetin-3-galactoside (Q-Ga), quercetin-3-rutinoside (Q-Ru), quercetin-3-glucoside (Q-Glu), kaempferol-3-rutinoside (K-Ru), kaempferol-3-glucoside (K-Glu) and derivative of quercetin produced in the reaction between quercetin-glucoside and p-coumaric acid (Q-Glu-p-CouA). Elemental analysis of quince seeds has not been performed previously. Also, using principal component and cluster analyses, we determined a strong negative relationship between total phenols and flavonoids, and Ni and Pb, specifically higher concentrations of these compounds were associated with lower concentrations of these metals.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.foodchem.2017.04.041DOI Listing

Publication Analysis

Top Keywords

acid
9
extracts quince
8
acid 5-cqa
8
quince
5
phenolic profiles
4
profiles metal
4
metal ions
4
ions analyses
4
analyses pulp
4
pulp peel
4

Similar Publications

Drug Development.

Alzheimers Dement

December 2024

Aptah Bio Inc., San Carlos, CA, USA.

Background: Alzheimer's disease (AD) is the most common cause of dementia worldwide. It is characterized by dysfunction in the U1 small nuclear ribonucleoproteins (snRNPs) complex, which may precede TAU aggregation, enhancing premature polyadenylation, spliceosome dysfunction, and causing cell cycle reentry and death. Thus, we evaluated the effects of a synthetic single-stranded cDNA, called APT20TTMG, in induced pluripotent stem cells (iPSC) derived neurons from healthy and AD donors and in the Senescence Accelerated Mouse-Prone 8 (SAMP8) model.

View Article and Find Full Text PDF

Background: Alzheimer's Disease (AD) is the leading form of senile dementia, affecting ∼6 million Americans and having a national economic impact of $321 billion, numbers expected to double by 2050. The major pathological hallmarks of AD include Amyloid Beta (Aβ) plaques and Tau neurofibrillary tangles (NFT). The first goal of this research was to develop novel forms of carbon dots (CD) using various precursors.

View Article and Find Full Text PDF

Background: Studies suggest a potential link between stroke and Alzheimer's disease wherein stroke may serve as a trigger for the onset or acceleration of Alzheimer's pathogenesis as damage to the brain's blood vessels may lead to the accumulation of amyloid beta protein which is a hallmark of Alzheimer's disease. Recent research has shown that stroke treatment may hold the key to treating Alzheimer's disease. The anti-inflammatory potentials of Cholinergic signaling are a novel therapeutic target in memory decline associated with Alzheimer's.

View Article and Find Full Text PDF

Background: Abnormal glucose metabolism in AD brains correlates with cognitive deficits. The glucose changes are consistent with brain thiamine (vitamin B1) deficiency. In animals, thiamine deficiency causes multiple AD-like changes including memory loss, neuron loss, brain inflammation, enhanced phosphorylation of tau, exaggerated plaque formation and elevated advanced glycation end products (AGE).

View Article and Find Full Text PDF

Background: Microbiota of the distal part of the intestine produces Urolithin A (Uro A) as a derivative of ellagitannins hydrolysis. Recently, the mitophagy, anti-inflammatory, and antioxidant properties of Uro A have focused more attention on its probable beneficial effects on neurodegenerative states. The purpose of this research was to study the impact of Uro A on the histopathology of the cerebellum in a rat model of streptozotocin-induced Alzheimer's disease.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!