Gluten contamination in labelled and naturally gluten-free grain products in southern India.

Consumption of a gluten-free diet or avoiding exposure to gluten is the only feasible and effective treatment available for coeliac patients to date. Although many grains and their products are naturally gluten-free, the possibility of gluten cross-contamination must be considered. Since such data are not available for Indian markets, we carried out this pilot study (n = 160) to assess gluten contamination in various grain-based food products from the category of breakfast products, flours, and batters made from grain that are naturally gluten free. The gluten was extracted from samples using 60% ethanol and gluten analysis was carried out using a commercially available competitive ELISA, which utilises a monoclonal antibody. Nearly 9.8% of the products labelled as gluten-free and 36.7% of the products made from naturally gluten-free grain were found to contain gluten above 20 mg/kg. Among products made from naturally gluten-free grain, 35.9% of the flour samples and 85% of the oat samples (11.67-1830 mg/kg) were contaminated with gluten. In the case of flours, unbranded samples collected from local markets (70%) and directly from local mills (30%) showed gluten content above Codex safety levels (20-400 mg/kg). Among products labelled as gluten free (n = 51), only 5 samples showed gluten contamination above 20 mg/kg although levels were well within 100 mg/kg (32.5 ± 5.8). Our study suggests that there is a likelihood of gluten contamination in products that are sourced from local retailers and millers.

Plasma paraoxonase1 activity in rats treated with monocrotophos: a study of the effect of duration of exposure.

We have earlier demonstrated the potential of monocrotophos (MCP), a highly toxic organophosphorus insecticide (OPI), to elicit insulin resistance in rats after chronic exposure. Given the understanding of role of paraoxonase1 (PON1) in OPI toxicity and diabetes pathology, this study was envisaged to understand the effect of duration of exposure to MCP on plasma PON1 activity in rats. Rats were administered MCP per os at 1/20 and 1/10th LD50 as daily doses for 180 days. Interim blood samples were collected at 15, 30, 45, 90 and 180 d for analysis of plasma parameters. Exposure to MCP for 45 resulted in persistent trend of hyperinsulinemia, while significant increase in fasting glucose levels was observed after 180 days. MCP caused suppression of plasma cholinesterase activity though the study period, albeit extent of inhibition was more severe during the early phase of the study. Exposure to MCP for 180 d resulted in hypertriglyceridemia and marginal decrease in HDL-C levels. MCP failed to modulate PON1 activity in plasma during the early phase of the study (up to 45 d). However, prolonged exposure resulted in significant increase in the plasma PON1 activity. This suggests that manifestation of insulin resistance in rats subjected to chronic exposure to MCP is associated with increase in PON1 activity. Our work provides rationale for studying whether the increase in PON1 activity observed in the present study serves to counter the deleterious effect of long term exposure to organophosphorus insecticides on metabolic homeostasis.

Hyperglycemic and stressogenic effects of monocrotophos in rats: evidence for the involvement of acetylcholinesterase inhibition.

The purpose of this study was to investigate the involvement of acetylcholinesterase (AChE) inhibition in hyperglycemic and stressogenic effects of monocrotophos in rats. Oral administration of monocrotophos (1.8 mg/kg b.w., 1/10 LD(50)) caused reversible hyperglycemia in rats with peak increase occurring at 2 h following administration. The hyperglycemic outcome at 2 h was accompanied by significant inhibition of acetylcholinesterase (AChE) activity in brain (84%), adrenal (68%) and liver (53%) and stressogenic effects as revealed by marked increase in plasma corticosterone (102%) and liver tyrosine aminotransferase (TAT) (104%) activity. At 4 h following administration, there was normalization of hyperglycemia and hypercorticosteronemia, marginal attenuation of liver TAT activity and marked increase in liver glycogen content, without spontaneous reactivation of AChE activity in the organs studied. Interestingly, pre-treatment of rats with acetylcholine (ACh) receptor antagonists-atropine sulfate and methyl atropine nitrate offered significant protection against hyperglycemia, hypercorticosteronemia and increased liver TAT activity induced by monocrotophos. Our results clearly demonstrate the involvement of AChE inhibition in hyperglycemia and stressogenic effects of monocrotophos in rats following acute exposure. Protection offered by both, general and peripheral ACh antagonists provide further evidence for the involvement of peripheral AChE inhibition in the monocrotophos-induced effects.

Microplate-based kinetic method for assay of mitochondrial NADH-- and succinate--cytochrome c reductase activities.

This article describes a microplate-based kinetic assay for mitochondrial NADH-- and succinate--cytochrome c reductase activities in rat brain mitochondria. The assay reported here is based on the conventional spectrophotometric method and involves substrate-driven reduction of exogenous cytochrome c. Conditions regarding linearity with respect to time and protein concentration have been standardized. Furthermore, the methods were tested for inhibition of respective activities by specific inhibitors. The microplate format described here can be employed for rapid and simultaneous measurements of mitochondrial NADH-- and succinate--cytochrome c reductase activities in a large number of samples.

Reversible hyperglycemia in rats following acute exposure to acephate, an organophosphorus insecticide: role of gluconeogenesis.

The present study was undertaken to investigate the hyperglycemic potential of acute exposure to acephate and its etiology employing rat model system. Oral administration of acephate (140mg/kg b.w.) caused reversible hyperglycemia as evidenced by peak increase in blood glucose at 2h after the administration (87% over control) followed by trend of normalization. In further experiment carried out to understand the etiology of the induced hyperglycemia, we observed that 2h exposure to acephate caused significant increase in blood glucose, plasma corticosterone (78%) and activities of two gluconeogenesis enzymes in liver viz., glucose-6-phosphatase (91%) and tyrosine aminotransferase (84%) compared to that in control. When rats were exposed to acephate for 6h, decrement was observed in elevated levels of blood glucose, plasma corticosterone and the gluconeogenesis enzymes of the liver. Adrenal cholesterol levels in acephate-exposed rats were significantly depleted. While the glycogen content in liver of 2-h exposure group was comparable to control, a tremendous increase in liver glycogen content ( approximately 3.5 folds) was observed in rats of the 6-h exposure group. Our results demonstrate that acephate causes reversible hyperglycemia in rats probably by enhancing hepatic glucose output via gluconeogenesis. A role for hyperactivity of adrenal cortex is suggested in increased gluconeogenesis while significant attenuation in elevated levels of blood glucose and the activity the gluconeogenesis enzyme, glucose-6-phosphatase in liver with concomitant increase in liver glycogen are indicative of the onset of counter-regulatory responses such as hyperinsulinemia, to overcome the induced hyperglycemia.