Snakebite is a severe medical, economic, and social problem across the world, mostly in the tropical and subtropical area. These regions of the globe have typical of the world's venomous snakes present where access to prompt treatment is limited or not available. Snake venom is a complex mixture of toxin proteins like neurotoxin and cardiotoxin, and other enzymes like phospholipase A2 (PLA2 ), haemorrhaging, transaminase, hyaluronidase, phosphodiesterase, acetylcholinesterase, cytolytic and necrotic toxins. Snake venom shows a wide range of biological effects like anticoagulation or platelet aggregation, hemolysis, hypotension and edema.Phospholipase A2 is the principal constituent of snake venom; it catalyzes the hydrolysis of the sn-2 position of membrane glycerophospholipids to liberate arachidonic acid, which is the precursor of eicosanoids including prostaglandins and leukotrienes. The information regarding the structure and function of the phospholipase A2enzyme may help in treating the snakebite victims. This review article constitutes a brief description of the structure, types, mechanism occurrence, and tests of phospholipase A 2 and role of components of medicinal plants used to inhibit phospholipase A2 .

Snakebite is a severe medical, economic, and social problem across the world, mostly in the tropical and subtropical area. These regions of the globe have typical of the world's venomous snakes present where access to prompt treatment is limited or not available. Snake venom is a complex mixture of toxin proteins like neurotoxin and cardiotoxin, and other enzymes like phospholipase A2 (PLA2 ), haemorrhaging, transaminase, hyaluronidase, phosphodiesterase, acetylcholinesterase, cytolytic and necrotic toxins. Snake venom shows a wide range of biological effects like anticoagulation or platelet aggregation, hemolysis, hypotension and edema.Phospholipase A2 is the principal constituent of snake venom; it catalyzes the hydrolysis of the sn-2 position of membrane glycerophospholipids to liberate arachidonic acid, which is the precursor of eicosanoids including prostaglandins and leukotrienes. The information regarding the structure and function of the phospholipase A2enzyme may help in treating the snakebite victims. This review article constitutes a brief description of the structure, types, mechanism occurrence, and tests of phospholipase A 2 and role of components of medicinal plants used to inhibit phospholipase A2 .

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