Toxicology International (Formerly Indian Journal of Toxicology)

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Flubendiamide and Lead Exposure Alters Glial Fibrillary Acidic Protein and Aspartic Acid Concentrations in Cerebrospinal Fluid in Buffalo Calves


Affiliations
1 Department of Veterinary Pharmacology and Toxicology, Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana, India
2 Department of Veterinary Medicine, Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana, India
     

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Changes in glial fibrillary acidic protein (GFAP) and aspartic acid (AA) concentrations in CSF following flubendiamide and lead exposure was studied. Male buffalo calves received daily oral dose of flubendiamide alone (n=4) @ 0.024mg/ kg/ day or lead acetate alone (n=4) @ 9.2 mg/ kg/ day or a combination of these two (n=4) for 90 days. Blood and CSF samples were collected and analyzed. GFAP in CSF did not alter in animals receiving flubendiamide alone. However, a significant increase in GFAP concentration in CSF was observed in animals receiving lead acetate. GFAP concentration showed a positive correlation (r = +0.545) with blood lead concentration in lead exposed animals, but no significant correlation was evident in animals exposed to both lead and flubendiamide. On the basis of results, it can be concluded that Aspartic acid concentration in CSF did not change significantly in lead treated animals, but increased significantly in flubendiamide treated animals. No significant alteration in AA level in CSF was observed in combined flubendiamide and lead treated animals. Flubendiamide exposure is associated with increase in AA level in CSF. Flubendiamide may have interactive effects with lead as evident from increase in GFAP and AA level in CSF after their combined exposure. This is the first report documenting alterations in GFAP and AA concentrations in CSF after flubendiamide exposure in mammals.

Keywords

CSF, Heavy Metal, Pesticide, Toxicity.
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  • Flubendiamide and Lead Exposure Alters Glial Fibrillary Acidic Protein and Aspartic Acid Concentrations in Cerebrospinal Fluid in Buffalo Calves

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Authors

Amita Ranjan
Department of Veterinary Pharmacology and Toxicology, Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana, India
V. K. Dumka
Department of Veterinary Pharmacology and Toxicology, Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana, India
R. Ranjan
Department of Veterinary Medicine, Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana, India
C. S. Randhawa
Department of Veterinary Medicine, Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana, India

Abstract


Changes in glial fibrillary acidic protein (GFAP) and aspartic acid (AA) concentrations in CSF following flubendiamide and lead exposure was studied. Male buffalo calves received daily oral dose of flubendiamide alone (n=4) @ 0.024mg/ kg/ day or lead acetate alone (n=4) @ 9.2 mg/ kg/ day or a combination of these two (n=4) for 90 days. Blood and CSF samples were collected and analyzed. GFAP in CSF did not alter in animals receiving flubendiamide alone. However, a significant increase in GFAP concentration in CSF was observed in animals receiving lead acetate. GFAP concentration showed a positive correlation (r = +0.545) with blood lead concentration in lead exposed animals, but no significant correlation was evident in animals exposed to both lead and flubendiamide. On the basis of results, it can be concluded that Aspartic acid concentration in CSF did not change significantly in lead treated animals, but increased significantly in flubendiamide treated animals. No significant alteration in AA level in CSF was observed in combined flubendiamide and lead treated animals. Flubendiamide exposure is associated with increase in AA level in CSF. Flubendiamide may have interactive effects with lead as evident from increase in GFAP and AA level in CSF after their combined exposure. This is the first report documenting alterations in GFAP and AA concentrations in CSF after flubendiamide exposure in mammals.

Keywords


CSF, Heavy Metal, Pesticide, Toxicity.

References





DOI: https://doi.org/10.22506/ti%2F2016%2Fv23%2Fi1%2F146666