Most synthetic coloured additives are carcinogenic; teratogenic and cause allergic reactions. In this study, the effects of synthetic azo dyes (sunset yellow FCF and carmoisine), as well as their degraded products (sulphanilic acid and naphthionic acid), on both true and pseudo-cholinesterases (ChEs) are studied. The results indicate that the synthetic azo dyes and their degraded products inhibit both human true and pseudo-ChE activities in vitro. The concentration of coloured additive that cause 50% inhibition (IC50) and enzyme inhibitor dissociation constant (Ki) show that sunset yellow FCF produces greater inhibition of both true and pseudo-ChEs than does carmoisine and sulphanilic acid, while naphthionic acid produces greater inhibition of pseudo-ChE only. Ki indicates that the affinity of sulphanilic acid for both true and pseudo-ChEs is higher than the other three inhibitors. Inhibition of both true and pseudo-ChEs by sunset yellow FCF is of mixed (competitive and non-competitive) type, but carmoisine and sulphanilic acid are non-competitive. Naphthionic acid produces a competitive inhibition kinetic with plasma ChE only. This inhibition is abolished by dialysis, indicating that their effects are reversible. The effects of sunset yellow FCF, carmoisine, sulphanilic acid and naphthionic acid on rat true and pseudo-ChEs are investigated. The data clearly show that there is a significant decrease in enzyme activity. Sulphanilic acid and sunset yellow FCF are the most potent in vivo inhibitors of true ChE and pseudo-ChE, respectively.
Hypertension (HT) affects about 20 percent of the adult population placing a high burden on health care systems. Cholinestrase is responsible of the hydrolysis of the vasodilator acetylcholine. Monoamine oxidase (MAO) is responsible for degradation of the vasoconstrictor biogenic amines. Nitric oxide synthase (eNOS) is responsible for the production of the vasodilator nitric oxide (NO). The study aimed to find the relationship between these enzymes and essential hypertension in recently diagnosed patients. The results indicated a significant decrease in the activity of pseudo ChE in HT patients compared to control resulting in increase of ACh content and also indicated a significant decrease in plasma MAO‐A in HT patients saving the biogenic amines. Similarly; there is a significant decrease in the plasma nitrites + nitrates [NOx] of HT patients due to decrease in NOS activity. Eventually; it could be concluded that the investigated enzymes played a role in the regulation of essential HT. As the study showed; increase of 5‐hydroxytryptamine and adrenaline (due to decrease in MAO) that exceeded the decrease of pseudo ChE (increasing ACh content) and NOS (decreasing NO) resulting in vasoconstriction exceeding vasodilatation and the blood pressure consequently rises. Reversal of the previous mechanism could be helpful in treating essential HT.
Grant Funding Source: Alexandria University
Dual inhibition of acetyl cholinestrase (AChE) and mono amine oxidase (MAO) types A and B in whole brain, cerebellum, basal ganglia, frontal cortex, pons and medulla oblongata of rat brain by aldicarb (2‐methyl‐2(methylthio) propionaldehyde O‐methyl(carbamoyl) oxime (C7H14O2NS) in vitro was studied. The inhibition of AChE and MAO types A and B in different parts of the brain was found to be of competitive type. The highest values of the enzyme inhibitor dissociation constant (Ki) were obtained with the extracts of pons and medulla oblongata, these parts responsible for vital centers (e.g. respiration). In case of MAO‐A the highest Ki values were obtained with the extracts of the cerebellum and frontal cortex, these parts responsible for balance and perception respectively. In case of MAO‐B the highest Ki value was obtained with the extract of basal ganglia, the part responsible for sense. The inhibition of the enzyme extracts by aldicarb was reversible, and the enzymes restored their whole activities by dialysis. The dual inhibition of AChE and MAO types A and B by the carbamate aldicarb save the neurotransmitters (e.g. acetylcholine and the biogenic amines) in the tissues especially in the nervous tissues, which are of great importance for Alzheimer dementia patients (AD).
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