Dichloroacetic acid-induced testicular toxicity in male rats and the protective effect of date fruit extract.

Background: The present study was designed to investigate the protective effect of aqueous date extract (ADE) against the dichloroacetic acid (DCA)-induced testicular injury in rats.

Methods: Forty-eight male Wistar rats were randomly divided into six groups of eight: group I served as the control; group II was given ADE (4 ml/kg) by gavage; groups III and IV received DCA at 0.5 and 2 g/L drinking water, respectively; and groups V and VI received DCA at 0.

Aqueous date fruit extract protects against lipid peroxidation and improves antioxidant status in the liver of rats subchronically exposed to trichloroacetic acid.

Trichloroacetic acid (TCA) is a prominent by-product of the chlorination of drinking water. It induces cell damage by producing free radicals and reactive oxygen species. The present study was carried out to evaluate the potential hepatoprotective role of the aqueous date extract (ADE) against TCA-induced liver injury.

Nephroprotective effect of date fruit extract against dichloroacetic acid exposure in adult rats.

The aim of this study was to investigate the protective effects of aqueous date extract (ADE) on dichloroacetic acid (DCA)-induced nephrotoxicity. In vitro, total phenolic content estimated in the ADE were 417.71mg gallic acid equivalents/100g fresh weights (FW), while total flavonoid and tannins contents were 285.

Oxidative damage and alterations in antioxidant enzyme activities in the kidneys of rat exposed to trichloroacetic acid: protective role of date palm fruit.

In this study, we investigated the antioxidant and protective properties of date fruit aqueous extract (DFAE) on trichloroacetic acid (TCA)-induced nephrotoxicity in rat. Oral administration of TCA as drinking water (0.5 and 2 g/L) daily for 2 months caused nephrotoxicity as evident by elevated levels of plasma creatinine, urea, and uric acid.

Protective effect of date palm fruit extract (Phoenix dactylifera L.) on dimethoate induced-oxidative stress in rat liver.

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.

Exploration of Pacific perspectives of Pacific models of mental health service delivery in New Zealand.

There is increasing concern about the inequalities, overall health outcomes, and mental health of Pacific peoples residing in New Zealand. The New Zealand Mental Health Survey (Te Rau Hinengaro), conducted in 2003/2004, identfied Pacific peoples as having a higher 12-month prevalence of mental disorders than the general population. The burden of mental health amongst Paqfic peoples was identified as high and associated with other socioeconomic correlates.

Spontaneous diabetes in hemizygous human amylin transgenic mice that developed neither islet amyloid nor peripheral insulin resistance.

Objectives: We sought to 1) Determine whether soluble-misfolded amylin or insoluble-fibrillar amylin may cause or result from diabetes in human amylin transgenic mice and 2) determine the role, if any, that insulin resistance might play in these processes.

Research Design And Methods: We characterized the phenotypes of independent transgenic mouse lines that display pancreas-specific expression of human amylin or a nonaggregating homolog, [(25,28,29)Pro]human amylin, in an FVB/n background.

Results: Diabetes occurred in hemizygous human amylin transgenic mice from 6 weeks after birth.

Regeneration of the heart in diabetes by selective copper chelation.

Heart disease is the major cause of death in diabetes, a disorder characterized by chronic hyperglycemia and cardiovascular complications. Although altered systemic regulation of transition metals in diabetes has been the subject of previous investigation, it is not known whether changed transition metal metabolism results in heart disease in common forms of diabetes and whether metal chelation can reverse the condition. We found that administration of the Cu-selective transition metal chelator trientine to rats with streptozotocin-induced diabetes caused increased urinary Cu excretion compared with matched controls.

Expression, crystallization and preliminary characterization of methylmalonyl coenzyme A epimerase from Propionibacterium shermanii.

Methylmalonyl-CoA epimerase (MMCE) is an enzyme that interconverts the R and S epimers of methylmalonyl-CoA in the pathway that links propionyl-CoA with succinyl-CoA. This is used for both biosynthetic and degradative processes, including the breakdown of odd-numbered fatty acids and some amino acids. The enzyme has been expressed in Escherichia coli both as the native enzyme and as its selenomethionine (SeMet) derivative.

Ultrastructural evidence that apoptosis is the mechanism by which human amylin evokes death in RINm5F pancreatic islet beta-cells.

A view is emerging that human amylin (HA) kills pancreatic islet beta-cells by apoptosis. This study strengthens this view by documenting time-dependent morphological and ultrastructural changes in 10 microm HA-treated cultured RINm5F islet beta-cells. Membrane blebbing and microvilli loss were the earliest detectable apoptosis-related phenomena, already evident 1 h after HA exposure.

Role of Ca2+ in apoptosis evoked by human amylin in pancreatic islet beta-cells.

The objective of these studies was to clarify the role of Ca(2+) in the mechanism of death evoked by human amylin (hA) in islet beta-cells. hA forms fibrils in vitro and islet amyloid in vivo. Here we show that pure synthetic hA aggregated in solution, formed fibrils and evoked death in cultured RINm5F islet beta-cells in a time-dependent (0-24 h) and concentration-dependent (0-20 microM) manner.

Induction of apoptosis by human amylin in RINm5F islet beta-cells is associated with enhanced expression of p53 and p21WAF1/CIP1.

Human amylin (10 microM) significantly inhibited RINm5F islet beta-cell proliferation and evoked apoptosis associated with typical degenerative ultrastructural changes and DNA fragmentation, whereas rat amylin did not. Time course analysis showed that human amylin elicited apoptosis in a passage-dependent manner. Expression of the apoptosis-related genes p53, bcl-2 and WAF1/CIP1 was examined using Northern blots.

Polymorphic fibrillar assembly of human amylin.

Human amylin forms fibrillar amyloid between pancreatic islet cells in patients with non-insulin-dependent (type 2) diabetes mellitus. Fibrillar assemblies also form in vitro in aqueous solutions of synthetic human amylin. We now report on the structural polymorphism of these fibrils.