| Description: |
Dextrose, a simple sugar (monosaccharide), is an important carbohydrate in biology, it exhibits marked antibacterial activity against Staphylococcus aureus,Escherichia coli and Pyocyanine. D-(+)-Glucose can prevent MPP+ toxicity, attenuate the loss of ATP, but do not reverse the complete inhibition of mitochondrial O2 consumption (MOC). |
| Targets: |
Antifection | ATP |
| In vitro: |
| Food Chem . 2015 May 15;175:485-93. | | D-glucose, D-galactose, and D-lactose non-enzyme quantitative and qualitative analysis method based on Cu foam electrode[Pubmed: 25577110] | | Abstract
Here, D-glucose, D-galactose, and D-lactose non-enzyme quantitative and qualitative analysis method using Cu foam electrode had been investigated. Porous Cu foam material was prepared by electrodeposition strategy, and used as working electrode. Cyclic voltammetry (CV) explained sweetener electro-oxidation process occurring on Cu foam electrode. Amperometric i-t scanning results demonstrated that Cu foam electrode fast responded to D-glucose, D-galactose, and D-lactose in linear concentration range between 0.18 mM and 3.47 mM with significant sensitivity of 1.79 mA cm(-2)mM(-1), 0.57 mA cm(-2)mM(-1), and 0.64 mA cm(-2)mM(-1), respectively. Limit of detection (LOD) was 9.30 μM, 29.40 μM, and 26 μM respectively (S/N=3). Sweetener species was decided by stochastic resonance (SR) signal-to-noise ratio (SNR) eigen peak located noise intensities. Interference experiment results demonstrated that Cu foam electrode selectively responded to sweeteners against interference chemicals. The proposed method provides a promising way for sweetener non-enzyme quantitative and qualitative analysis.
Keywords: Cu foam; Non-enzyme; d-Galactose; d-Glucose; d-Lactose. |
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| In vivo: |
| Brain Research Volume 962, Issues 1–2, 7 February 2003, Pages 48–60 | | d-(+)-Glucose rescue against 1-methyl-4-phenylpyridinium toxicity through anaerobic glycolysis in neuroblastoma cells[Reference: WebLink] | The active neurotoxin of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 1-methyl-4-phenylpyridinium (MPP+), exerts its lethal effect by inhibiting Complex I of the electron transport chain (ETC). MPP+ shuts down aerobic oxidative phosphorylation and ETC-mediated ATP synthesis.
METHODS AND RESULTS:
The present investigation examines anaerobic survival during MPP+ toxicity in murine neuroblastoma cells Neuro 2-A (N2-A). MPP+ addition to the cells resulted in a reduction in cell viability, mitochondrial O2 consumption (MOC) and ATP concentration in a dose-dependent manner. However, the addition of 10 mM of d-(+)-glucose prevented MPP+ toxicity, attenuated the loss of ATP, but did not reverse the complete inhibition of MOC, indicating substrate level phosphorylation and explicit anaerobic survival. Glucose addition prevented MPP+-mediated drop in ΔΨm, endoplasmic reticulum and intracellular organelle membrane potential tantamount to an increase of cell viability. Secondly, we examined the metabolic regulation of pyruvate dehydrogenase (PDH) and carnitine palmitoyl transferase (CPT) activities during glucose rescue. These enzymes exert control over acetyl CoA reservoirs in the mitochondria during aerobic metabolism. dl-6,8-Thioctic acid (PDH prosthetic group) and insulin slightly augmented metabolic rate, resulting in enhanced vulnerability to MPP+ in a glucose-limited environment. Additional glucose prevented these effects. Amiodarone (CPT inhibitor) and glucagon did not hamper or potentiate glucose rescue against MPP+. These data support strict anaerobic glucose utilization in the presence of toxic levels of MPP+. Moreover, the findings indicate that MPP+ exerts two distinct modes of toxicity (fast and slow death). With MPP+ (<1 mM), anaerobic glycolysis is operational, and toxicity is strictly dependent upon glucose depletion. MPP+ (1–10 mM) initiated acute metabolic collapse, with failure to sustain or switch to anaerobic glycolysis.
CONCLUSIONS:
In conclusion, overcoming energy failure against MPP+ may involve targeting rate-limiting controls over anaerobic energy pathways. |
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