Evaluation of the toxic potential of Bisphenol-A glycidylmethacrylate (BisGMA) on the third instar larvae of transgenic Drosophila.

Introduction: In the present study the cytotoxic and genotoxic effects of Bisphenol-A glycidyl methacrylate (BisGMA) was studied on the third instar larvae of transgenic Drosophila melanogaster (hsp70-lacZ)Bg9. Materials and methods: The concentration of BisGMA i.e. 0.005, 0.010, 0.015 and 0.020 M were established in diet and the larvae were allowed to feed on it for 24 h. Results: A dose dependent significant increase in the activity of ß-galactosidase was observed compared to control. A significant dose dependent tissue damage was observed in the larvae exposed to 0.010, 0.015 and 0.020 M of BisGMA compared to control. A dose dependent significant increase in the Oxidative stress markers was observed compared to control. BisGMA also exhibit significant DNA damaged in the third instar larvae of transgenic D. melanogaster (hsp70-lacZ)Bg9 at the doses of 0.010, 0.015 and 0.020 M compared to control. Conclusion: BisGMA at 0.010, 0.015 and 0.020 M was found to be cytotoxic for the third instar larvae of transgenic D. melanogaster (hsp70-lacZ) Bg9.

Effect of Apigenin on Neurodegenerative Diseases.

Neurodegenerative diseases (NDDs), such as Alzheimer's and Parkinson's, are the most frequent age-related illnesses affecting millions worldwide. No effective medication for NDDs is known to date and current disease management approaches include neuroprotection strategies with the hope of maintaining and improving the function of neurons. Such strategies will not provide a cure on their own but are likely to delay disease progression by reducing the production of neurotoxic chemicals such as reactive oxygen species (ROS) and related inflammatory chemicals. Natural compounds such as flavonoids that provide neuroprotection via numerous mechanisms have attracted much attention in recent years. This review discusses evidence from different research models and clinical trials on the therapeutic potential of one promising flavonoid, apigenin, and how it can be helpful for NDDs in the future prospects. We have also discussed its chemistry, mechanism of action, and possible benefits in various examples of NDDs.

Evaluation of Bis(2-ethylhexyl) phthalate toxicity on the third instar larvae of transgenic Drosophila melanogaster (hsp70-lacZ) Bg9.

Bis(2-ethylhexyl) phthalate, generally known as DEHP is a synthetic compound mainly used as a plasticizer to make polyvinyl chloride products flexible and soft. The present work aimed to study the toxicity of Bis(2-ethylhexyl) phthalate on the third instar larvae of transgenic Drosophila melanogaster(hsp70-lacZ) Bg9. The hsp70 gene is associated with the ß-galactosidase in our present transgenic strain therefore, the more activity of ß-galactosidase will indirectly correspond to hsp70 expression. The third instar larvae were allowed to feed on the diet for 24 h having 0.001, 0.005, 0.01, and 0.02 M of Bis(2-ethylhexyl) phthalate at the final concentration. After the exposure of 24hrs, the larvae were subjected to ONPG assay, X-gal staining, trypan blue exclusion test, oxidative stress markers assays, and comet assay. A dose-dependent increase in hsp70 expression, tissue damage, Glutathione-S-transferase (GST) activity, lipid peroxidation, monoamine oxidase, caspase-9 & 3, protein carbonyl content (PCC), DNA damage and decrease in the glutathione (GSH) content, delta-aminolevulinic acid dehydrogenase (ẟ-ALD-D) and acetylcholinesterase activity were observed in the larvae exposed to 0.005, 0.01, 0.02 M of Bis-(2-ethylhexyl) phthalate. The dose of 0.001 M of Bis(2-ethylhexyl) phthalate did not showed any toxic effects and hence can be considered as No Observed Adverse Effect Level (NOAEL) for Bis(2-ethylhexyl) phthalate. The study supports the use of Drosophila for the evaluation of possible toxic effects associated with synthetic compounds.

Beneficial effects of apigenin on the transgenic Drosophila model of Alzheimer's disease.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder. The available drugs improve the symptoms but do not play role in modifying disease effects. Currently, the treatment strategies focus on inhibiting the production of Aß-42 aggregates and tau filaments. In this context the natural plant products could act as a potent candidate. Therefore, we decided to study the effect of apigenin on the transgenic Drosophila model of AD i.e., expressing Aß-42 in the neurons. The AD flies were allowed to feed on the diet having 25, 50, 75 and 100 µM of apigenin for 30 days. The exposure of AD flies to apigenin showed a dose dependent significant decrease in the oxidative stress and delay in the loss of climbing ability. Apigenin also inhibits the activity of acetylcholinesterase. The immunostaining and molecular docking studies suggest that apigenin inhibits the formation of Aß-42 aggregates. Apigenin is potent in reducing the AD symptoms being mimicked in the transgenic Drosophila model of AD.