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Modulation of monoamine oxidase activity in different brain regions and platelets following exposure of rats to methylmercury.
Toxicity and bioaccumulation of nickel sulfate in Sprague-Dawley rats following 13 weeks of subchronic exposure.
- E. Obone, S. Chakrabarti, C. Bai, M. Malick, L. Lamontagne, K. S. Subramanian
- MedicineJournal of Toxicology and Environmental Health…
- 23 July 1999
Both immune and pulmonary systems were found to be very sensitive targets, followed by kidney, in terms of order of toxicity, and nickel sulfate-treated rats were the most vulnerable to such targets.
Role of oxidative stress in nickel chloride-induced cell injury in rat renal cortical slices.
DNA-protein crosslinks induced by nickel compounds in isolated rat lymphocytes: role of reactive oxygen species and specific amino acids.
- S. Chakrabarti, C. Bai, K. S. Subramanian
- Biology, ChemistryToxicology and Applied Pharmacology
- 1 February 2001
Deferoxamine (a highly specific iron chelator) treatment prevented nickel subsulfide-induced DNA-protein crosslink formation, suggesting that Ni(2+)-induced DPXL formation in rat lymphocytes is caused by the induction of Fenton/Haber-Weiss reaction, generating hydroxyl radicals.
Genotoxic effects of chromium(VI) and cadmium(II) in human blood lymphocytes using the electron microscopy in situ end-labeling (EM-ISEL) assay.
Studies of acute nephrotoxic potential of trichloroethylene in Fischer 344 rats.
It is demonstrated that TRI exerts its acute nephrotoxic potential at a very high dose level and produces neph rotoxic insult at the proximal tubular and possibly glomerular regions of the rat kidney, whether exposed by inhalation or by an ip route.
Role of oxidative stress, mitochondrial membrane potential, and calcium homeostasis in nickel sulfate-induced human lymphocyte death in vitro.
DNA-Protein crosslinks induced by nickel compounds in isolated rat renal cortical cells and its antagonism by specific amino acids and magnesium ion.
The potent protective effects of these specific amino acids and Mg2+ against nickel subsulfide-induced DNA-protein crosslink formation in isolated renal cortical cells are due to reduction of cellular uptake of Ni2+ and inhibition of the binding ofNi2+ to deproteinized DNA.
Role of oxidative stress and intracellular calcium in nickel carbonate hydroxide-induced sister-chromatid exchange, and alterations in replication index and mitotic index in cultured human peripheral…
Overall these data indicate that various types of oxidative stress including iron-mediated oxidative stress involving the Fenton–Haber/Weiss reaction, and alterations in calcium homeostasis are involved in the genetic damage produced by the soluble form of NiCH.
Role of oxidative stress, mitochondrial membrane potential, and calcium homeostasis in human lymphocyte death induced by nickel carbonate hydroxide in vitro
- Prosper M'bemba-meka, N. Lemieux, S. Chakrabarti
- Biology, ChemistryArchives of Toxicology
- 26 April 2006
The mechanism of NiCH (soluble form)-induced activation of lymphocyte death signalling pathways involves not only the excess generation of different types of oxidative stress, but also the induction of alteration in ΔΨm and destabilization of cellular calcium homeostasis as well.