Impact of quinalphos on blood glucose and acetylcholinesterase (AChE) activity in brain and pancreas in a roseringed parakeet (Psittacula krameri borealis: Newmann)

Anam, Kamrul; Maitra, Saumen Kumar

doi:10.1007/bf00213081

Cited by 17 publications

(9 citation statements)

References 22 publications

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“…These changes could be related to possible inhibition or decreased cholinergic activity on exposure to quinalphos. Since, quinalphos is a potent neurotoxic agent which inhibits acetyl cholinesterase activity of brain [37]. Similarly, membrane bound K 1+ , Mg 1+ ATPase and Ca 2+ ATPase activities have been decreased in dose and time depend manner in the brain regions (hen mesencephalon, cerebellum and medulla oblongata) of the fish Oreochromis mocsombicus [38], which supports the histological changes observed in the brain of Cyprinus Carpio in the present study.…”

Section: Discussionsupporting

confidence: 88%

Histopathological Alterations in the Gill, Liver and Brain of Cyprinus Carpio on Exposure to Quinalphos

Chamarthi¹,

Manjunatha²,

Gooty

et al. 2014

AJLS

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Study was conducted to assess the histopathological damage of Gill, Liver and Brain in common carp, Cyprinus carpio after sublethal exposure to Quinalphos. Exposed to sublethal concentration (One tenth (1/10th, 0.75 µl/L) of commercial grade quinalphos (25% Emulsified Concentration) for 1, 7, 14, 21 and 30 days and a parallel control was run simultaneously. Gill, Liver and Brain of exposed individuals exhibited some remarkable changes in their histology in comparison to control. Prominent changes include shrinkage of the glomerulus, and dilation of tubular lumen. Vacuolization, desquamation, hydropic swelling and hyaline degeneration of tubular epithelium is also observed. Cyst formation and hemorrhage also appear in certain specimens. Duration of exposure appears to have a profound effect on Gill, Liver and Brain as with increasing duration of exposure histopathological damages become more severe.

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Section: Discussionsupporting

confidence: 88%

Histopathological Alterations in the Gill, Liver and Brain of Cyprinus Carpio on Exposure to Quinalphos

Chamarthi¹,

Manjunatha²,

Gooty

et al. 2014

AJLS

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“…Hyperglycemic effect has also been reported in experimental animals following to acute and chronic OPI exposures (Begum and Vijayaraghavan, 1999;Sarin and Gill, 1999;Abdollahi et al, 2004b;Pournourmohammadi et al, 2005). Hyperglycemia has been known to occur as a consequence of increased accumulation of acetylcholine (ACh) at the nerve endings following AChE inhibition (Anam and Maitra, 1995). ACh, the major parasympathetic neurotransmitter, is released from intra pancreatic nerve endings.…”

Section: Discussionmentioning

confidence: 97%

Altered glucose homeostasis and oxidative impairment in pancreas of rats subjected to dimethoate intoxication

Kamath

Rajini

2007

Toxicology

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“…For better understanding, readers are requested to focus on the Figures 2 and 3, and study the summarized information of all papers that appeared in Table 1 even those that have not been cited inside text. [207][208][209][210][211][212][213][214][215][216][217][218][219][220][221][222]…”

Section: Discussionmentioning

confidence: 99%

Toxic influence of organophosphate, carbamate, and organochlorine pesticides on cellular metabolism of lipids, proteins, and carbohydrates

2010

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Pesticides, including organophosphate (OP), organochlorine (OC), and carbamate (CB) compounds, are widely used in agricultural and indoor purposes. OP and CB act as acetyl cholinesterase (AChE) inhibitors that affect lots of organs such as peripheral and central nervous systems, muscles, liver, pancreas, and brain, whereas OC are neurotoxic involved in alteration of ion channels. There are several reports about metabolic disorders, hyperglycemia, and also oxidative stress in acute and chronic exposures to pesticides that are linked with diabetes and other metabolic disorders. In this respect, there are several in vitro and in vivo but few clinical studies about mechanism underlying these effects. Bibliographic databases were searched for the years 1963–2010 and resulted in 1652 articles. After elimination of duplicates or irrelevant papers, 204 papers were included and reviewed. Results indicated that OP and CB impair the enzymatic pathways involved in metabolism of carbohydrates, fats and protein within cytoplasm, mitochondria, and proxisomes. It is believed that OP and CB show this effect through inhibition of AChE or affecting target organs directly. OC mostly affect lipid metabolism in the adipose tissues and change glucose pathway in other cells. As a shared mechanism, all OP, CB and OC induce cellular oxidative stress via affecting mitochondrial function and therefore disrupt neuronal and hormonal status of the body. Establishing proper epidemiological studies to explore exact relationships between exposure levels to these pesticides and rate of resulted metabolic disorders in human will be helpful.

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Impact of quinalphos on blood glucose and acetylcholinesterase (AChE) activity in brain and pancreas in a roseringed parakeet (Psittacula krameri borealis: Newmann)

Cited by 17 publications

References 22 publications

Histopathological Alterations in the Gill, Liver and Brain of Cyprinus Carpio on Exposure to Quinalphos

Histopathological Alterations in the Gill, Liver and Brain of Cyprinus Carpio on Exposure to Quinalphos

Altered glucose homeostasis and oxidative impairment in pancreas of rats subjected to dimethoate intoxication

Toxic influence of organophosphate, carbamate, and organochlorine pesticides on cellular metabolism of lipids, proteins, and carbohydrates

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