The objectives of this hospital based cross-sectional study were to evaluate the socio-demographic profile, manner of death and histopathological changes in the lungs, liver and kidneys of individuals who died of pesticide poisoning. All fatal cases of pesticide poisoning from February 2011 to January 2012 were evaluated. Socio-demographic profile, type of exposure and manner of death were recorded for each of the cases. Autopsy was performed with detailed internal and external examinations. Random portion of Lung, Liver and Kidney were collected and fixed in 10.0% Formalin. Hematoxylin and Eosin stained sections were examined and findings recorded. The total number of deaths due to fatal pesticide poisoning was 9.6%. Highest frequency of poisoning (23.4%) was seen in the age group 20 - 29 years. The peak time of consumption of poisoning was between 6.00am and 12.00noon. The manner of poisoning was suicidal in majority of the cases. Histological findings indicated that congestion was the most common histopathological change; being observed in 60.0%, 66.0% and 74.0% of cases of liver, lung and kidney respectively. Histopathological features are supportive in establishing the diagnosis but further studies with larger sample size may be more illuminative in explaining the histopathological changes occurring due to these chemicals.

OBJECTIVE: In this study, the combined effect of two stressors, namely, electromagnetic fields (EMFs) from mobile phones and fructose consumption, on hypothalamic and hepatic master metabolic regulators of the AMPK/SIRT1-UCP2/FOXO1 pathway were elucidated to delineate the underlying molecular mechanisms of insulin resistance. METHODS: Weaned Wistar rats (28 days old) were divided into 4 groups: Normal, Exposure Only (ExpO), Fructose Only (FruO), and Exposure and Fructose (EF). Each group was provided standard laboratory chow ad libitum for 8 weeks . Additionally, the control groups, namely, the Normal and FruO groups, had unrestricted access to drinking water and fructose solution (15%), respectively. Furthermore, the respective treatment groups, namely, the ExpO and EF groups, received EMF exposure (1,760 MHz, 2 h/day x 8 weeks). In early adulthood, mitochondrial function, insulin receptor signaling, and oxidative stress signals in hypothalamic and hepatic tissues were assessed using western blotting and biochemical analysis. RESULT: In the hypothalamic tissue of EF, SIRT1, FOXO 1, p-PI3K, p-AKT, Complex III, UCP2, MnSOD, and catalase expressions and OXPHOS and GSH activities were significantly decreased ( P < 0.05) compared to the Normal, ExpO, and FruO groups. In hepatic tissue of EF, the p-AMPKα, SIRT1, FOXO1, IRS1, p-PI3K, Complex I, II, III, IV, V, UCP2, and MnSOD expressions and the activity of OXPHOS, SOD, catalase, and GSH were significantly reduced compared to the Normal group ( P < 0.05). CONCLUSION The findings suggest that the combination of EMF exposure and fructose consumption during childhood and adolescence in Wistar rats disrupts the closely interlinked and multi-regulated crosstalk of insulin receptor signals, mitochondrial OXPHOS, and the antioxidant defense system in the hypothalamus and liver.
Humans ; Rats ; Animals ; Adult ; Rats, Wistar ; Fructose/metabolism* ; Catalase ; Receptor, Insulin/metabolism* ; AMP-Activated Protein Kinases/metabolism* ; Electromagnetic Fields/adverse effects* ; Sirtuin 1/metabolism* ; Cell Phone ; Phosphatidylinositol 3-Kinases/metabolism* ; Forkhead Box Protein O1/metabolism* ; Uncoupling Protein 2