Post by beebs on Nov 30, 2011 17:11:23 GMT -5
A while ago, someone offered me a date. I ate about a dozen and noticed an improvement in continuous arrythmias. Curious, I started reading about compounds, and nutrients it contained. Suprisingly, high amount of potassium, magnesium and other nutrients such as thiamine and more. Could it be I am deficient in minerals and other nutrients, most probably.
Fast forward, stumbled on two great articles about compounds in dates which helps liver toxicity and are neuro-protective. Chinese and Ayurvedic medicine use dates for various ailments. The Chinese soak specific dates in glutinous rice overnight, cook and eat the following day, beneficial for cardiac issues too.
Exp Toxicol Pathol. 2011 Jul;63(5):433-41. Epub 2010 Mar 31.
Protective effect of date palm fruit extract (Phoenix dactylifera L.) on dimethoate induced-oxidative stress in rat liver.
Saafi EB, Louedi M, Elfeki A, Zakhama A, Najjar MF, Hammami M, Achour L.
Source
Laboratoire de Biochimie, UR Nutrition Humaine et Désordres Métaboliques, Faculté de Médecine, 5000 Monastir, Tunisia.
Abstract
Nowadays, people's exposure to chemical compounds such as organophosphorus insecticides is continuously on the rise more and more. Theses compounds have induced an excessive production of free radicals which are responsible for several cell alterations in the organism. Recent investigations have proved the crucial role of nutritional antioxidants to prevent the damage caused by toxic compounds. In this study, we investigate the role of date palm fruit extract (Phoenix dactylifera L.) in protection against oxidative damage and hepatotoxicity induced by subchronic exposure to dimethoate (20mg/kg/day). Oral administration of dimethoate caused hepatotoxicity as monitored by the increase in the levels of hepatic markers enzymes (transaminases, alkaline phosphatase, gamma-glutamyl transferase and lactate dehydrogenase), as well as in hepatic malondialdehyde thus causing drastic alteration in antioxidant defence system. Particularly, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) were found increased by dimethoate while catalase (CAT) activity was reduced significantly. These biochemical alterations were accompanied by histological changes marked by appearance of vacuolization, necrosis, congestion, inflammation, and enlargement of sinusoids in liver section. Pretreatment with date palm fruit extract restored the liver damage induced by dimethoate, as revealed by inhibition of hepatic lipid peroxidation, amelioration of SOD, GPx and CAT activities and improvement of histopathology changes. The present findings indicate that in vivo date palm fruit may be useful for the prevention of oxidative stress induced hepatotoxicity.
Copyright © 2010 Elsevier GmbH. All rights reserved.
www.ncbi.nlm.nih.gov/pubmed/20359872
Indian J Exp Biol. 2011 Aug;49(8):627-33.
Evaluation of antioxidant and neuroprotective effect of date palm (Phoenix dactylifera L.) against bilateral common carotid artery occlusion in rats.
Pujari RR, Vyawahare NS, Kagathara VG.
Source
Department of Pharmacology, AISSMS College of Pharmacy, Kennedy Road, Near RTO, Pune-411 001, India. rohinipujari@yahoo.com
Abstract
The cerebral ischemia in rats was induced by occluding bilateral common carotid arteries (BCCAO) for 30 min., followed by 45 min reperfusion. BCCAO caused significant depletion in superoxide dismutase, catalase, glutathione, glutathione peroxidase, glutathione-S-transferase, glutathione reductase and significant increase in lipid peroxidation along with severe neuronal damage in the brain. All the alterations except depletion in glutathione peroxidase and glutathione-S-transferase levels induced by cerebral ischemia were significantly attenuated by 15 days pretreatment with methanolic extract of P. dactylifera fruits (100, 300 mg/kg), whereas 30 mg/kg dose was insignificant in this regard. These results suggest the possible use P. dactylifera against bilateral common carotid artery occlusion induced oxidative stress and neuronal damage.
www.ncbi.nlm.nih.gov/pubmed/21870431