Informatics Publishing Limited

Arnab Roy ¹, Moutushi Mandi ¹, Sumedha Roy ¹

Affiliations
1 Toxicology Research Unit, Cytogenetics Laboratory, Department of Zoology, The University of Burdwan, Burdwan, West Bengal, IN

Abstract

Rotenone is a widely used natural pesticide and piscicide and a potent inhibitor of mitochondrial complex I (NADHquinone reductase) that elicits the degeneration of dopaminergic neurons. Present study explored the adverse effect of rotenone at concentrations far below the reported LC₅₀ on several life cycle parameters and on the compound eye structure of a non-target insect, Drosophila melanogaster. Newly hatched first instar larvae were introduced in Drosophila food medium containing different concentrations (50, 100, 150, 200, 250 μg/L) of rotenone. Different life cycle parameters were recorded. Emerged adult flies were collected and studied under Scanning electron microscope. Student's t-test was performed to explore significant difference and changes in both life cycle parameter and eye architecture. Treated groups showed significant delay (p<0.05 level) in larval duration, pupal duration, and in emergence of flies when compared with the control groups. Delay in life cycle parameters significantly increased with increase of rotenone exposure. Interestingly, the compound eye structure of the treated flies was seen to be affected by rotenone. Thus these results clearly demonstrate that chronic exposure to rotenone can alter the structure and lifecycle of a non-target organism like Drosophila at sub-lethal concentrations. Thus rotenone in Drosophila at sub-lethal concentrations might be the reason for developmental toxicity.

Keywords

Rotenone, Drosophila, Ommatidia, SEM.

Full Text

     

Prem Rajak ¹, Moutushi Mandi ², Anik Dutta ³, Sumedha Roy ²

Affiliations
1 Department of Zoology, A. B. N. Seal College, Cooch Behar, West Bengal, IN
2 Toxicology Research Laboratory, Department of Zoology, The University of Burdwan, Purba Bardhaman, West Bengal, IN
3 Department of Zoology, Darjeeling Government College, Darjeeling, West Bengal, IN

Abstract

Drosophila is a versatile model organism to study metabolic disorders, one such being diabetes mellitus. Eight insulin-like peptides (ILPs) have been identified in Drosophila. ILPs are produced from paired Insulin-producing cells present in brain ganglia. Another protein called adipokinetic hormone (AKH) is homologous to mammalian glucagon and is released from the corpora cardiaca. Synergistic action of ILP and AKH maintains sugar homeostasis in Drosophila. ILP binds with insulin receptors on the adipocytes and trigger autophosphorylation and dimerization. The activated receptors then initiate a downstream signaling by various modulators to phosphorylate Akt (protein kinase B, a serine-threonine-specific protein kinase). Akt, when activated, targets multiple signaling molecules including Target of Rapamycin (TOR) that participates in glucose metabolism, protein synthesis, cell proliferation, neuroendocrine signaling, and stress response. Akt also phosphorylates transcription factor FOXO that promotes cell survival by up-regulating TRAIL, a pro-apoptotic protein. High lipid accumulation in the fat body is linked with insulin resistance in Drosophila. Drosophila reared on high lipid diet shows up-regulation in protein kinase C (PKC). PKC is known to antagonize insulin signaling in fruit flies. A clear concept regarding the complex process of glucose homeostasis can be generated through further investigations. Since Drosophila has several advantages over vertebrate models, it can be used to identify additional modulators of insulin biology and metabolism.

Keywords

Akt, Drosophila, FOXO, Insulin-Like Peptides, TOR.

Full Text

     

Prem Rajak ¹, Sumedha Roy ², Abhratanu Ganguly ¹, Moutushi Mandi ³, Anik Dutta ⁴, Saurabh Sarkar ⁵, Sayantani Nanda ¹, Salma Khatun ⁶, Siddhartha Ghanty ¹, Gopal Biswas ³

Affiliations
1 Department of Animal Science, Kazi Nazrul University, Asansol, West Bengal - 713340, IN
2 Cytogenetics Laboratory, Department of Zoology, The University of Burdwan, West Bengal - 713104, IN
3 Toxicology Research Unit, Department of Zoology, The University of Burdwan, Purba Bardhaman, West Bengal - 713104, IN
4 Post Graduate, Department of Zoology, Darjeeling Govt. College, Darjeeling, West Bengal - 734104, IN
5 Department of Zoology, Gushkara Mahavidyalaya, Gushkara, West Bengal - 713128, IN
6 Krishna Chandra College, Hetampur, Birbhum, West Bengal - 731124, IN

Abstract

Pesticides are an integral part of our daily life, used in agricultural fields, store rooms, residences and educational institutions to kill or repel pests. Several chemical subtypes of these compounds are available, of which organophosphate (OP) is major one. These are broad spectrum pesticides used to kill insect pests. OPs are useful but indeed they are most frequent reasons of pesticide poisoning across the globe. OP inhibits acetylcholinesterase activities that results in continuous hyper-excitable state of nicotinic and muscarinic receptors at neuromuscular junctions. Intentional or unintentional exposure to OPs causes abdominal pain, diarrhea, vomiting, muscular weakness, dementia, Central Nervous System (CNS) dysfunction and even death. Besides acetylcholinesterase inhibition, OPs are also known to trigger ROS generation within the cellular machinery which results in Oxidative Stress (OS). Free Radicals (FRs) are neutralized by antioxidant-defense system of the body. Vitamin C and vitamin E are the major exogenous antioxidants that scavenge a large amount of free radicals by donating their own electrons to FRs. This phenomenon reduces ROS and hence, OS is prevented. Therefore, vitamin C and E can be considered for daily dietary intake which might be providing prophylactic advantage against OP induced OS and pathophysiology in human beings.

Keywords

Ascorbic Acid, Organophosphates, Oxidative Stress, ROS, Tocopherol

Full Text

   

Prem Rajak ¹, Sumedha Roy ², Salma Khatun ³, Moutushi Mandi ⁴, Abhratanu Ganguly ¹, Kanchana Das ⁴, Anik Dutta ⁵, Sayantani Nanda ¹, Siddhartha Ghanty ¹, Gopal Biswas ⁴

Affiliations
1 Department of Animal Science, Kazi Nazrul University, Asansol – 713340, West Bengal, IN
2 Cytogenetics Laboratory, Department of Zoology, The University of Burdwan, Purba Bardhaman – 713104, West Bengal, IN
3 Department of Zoology, Krishna Chandra College, Hetampur – 731124, West Bengal, IN
4 Toxicology Research Unit, Department of Zoology, The University of Burdwan, Purba Bardhaman – 713104, West Bengal, IN
5 Post Graduate Department of Zoology, Darjeeling Government College, Darjeeling –734104, West Bengal, IN

Abstract

Fluoride is the thirteenth most abundant element in the earth’s crust. It is highly electronegative and distributed ubiquitously in nature. During weathering of rocks and soil, fluoride can leach out and dissolve in the groundwater. Both plants and animals are exposed to several compounds of fluoride through contaminated soil and water. Fluoride contamination in groundwater is a major global concern as groundwater is frequently used for drinking in various parts of the world, especially in developing countries. Fluoride compounds have been reported to impose acute and chronic health hazards. Millions of global populations are suffering from dental and skeletal fluorosis due to high fluoride intake through drinking water. In green vegetation, fluoride accumulation causes necrosis in the tip and marginal portions of leaves. Diverse detrimental effects of fluoride on health have insisted researchers globally to identify compounds having protective potential against fluoride toxicity. Several plant extracts, vitamins, polyphenols, melatonin, hypophyseal proteins, and lycopene have been demonstrated to enhance the antioxidant status and subvert fluoride-induced health hazards in model organisms. However, more studies are required to forward conclusive opinions in terms of the real-life efficacy of these antioxidants against fluoride toxicity.

Keywords

Selected:Fluoride, Fluorosis, Lycopene, Melatonin, Oxidative Stress.Remove Fluoride, Fluorosis, Lycopene, Melatonin, Oxidative Stress.

Full Text