Toxicant-induced

Hirose A, Takagi A, Nishimura T, Ema M (2004) Review of reproductive and developmentai toxicity induced by organotins in aquatic organisms and experimentai animais. Organohalogen Compounds, 66 3042-3047. 

Khan PK, Sinha SP. 1996. Ameliorating effect of vitamin C on murine sperm toxicity induced by three pesticides (endosulfan, phosphamidon and mancozeb). Mutagenesis ll(l) 33-36. 

DNA damage by trans-2,4-NjP-, (NC H ) (NHMe) occurs via cross-linking while with trans-2,6-N P (NC H ) (NHMe) both single strand breaking and cross-linking occurs. Although cumulative bone marrow toxicity induced by 2,2-N P2(IK H)4(pYr)2 (Pyr=pyrroli-... 

Trosko, J. E., C. C. Chang, B. Upham, and M. Wilson. 1998. Epigenetic toxicology as toxicant-induced changes in intracellular signalling leading to altered gap junctional intercellular communication. Toxicol Lett 102-103 71-78. 

Intratracheal instillation Inhalation 24 d Pulmonary toxicity induced only by intratracheal instillation [75]... 

Tutak, W. et al. (2009) Toxicity induced enhanced extracellular matrix productionin osteoblastic cells cultured on single-walled carbon nanotube networks. Nanotechnology, 20 (25). 255101. 

Jensen, K.F., Olin, J., Haykal-Coates, N., O Callaghan, J., Miller, D.B., and de Olmos, J.S., Mapping toxicant-induced nervous system damage with a cupric silver stain a quantitative analysis of neural degeneration induced by 3,4-methylenedioxymethamphetamine, NIDA Res. Monogr. 136, 133-149 discussion 150-154, 1993. 

Renal toxicity induced by penicillamine is usually manifested as reversible proteinuria and hematuria, but may progress to nephrouritic syndrome with membraneous glomerulopathy. 

Tousignan JD, Gates AL, Ingram LA et al (2002) Comprehensive analysis of the acute toxicities induced by systemic administration of cationic lipid Plasmid DNA complexes in mice. Hum Gene Ther 11 2493-2513... 

Heck, H. d A., M. Casanova, M.J. McNulty, and C.W. Lam. 1986. Mechanisms of nasal toxicity induced by formaldehyde and acrolein. Pages 235-247 in C.S. Barrow (ed.). Toxicology of the Nasal Passages. Hemisphere Publishing, New York. 

Immunotoxicity testing in rodents exposed to industrial and/or environmental chemicals, has been recognized as an important toxicological concern for over 25 years. Early immunotoxicity testing relied primarily on the mouse, due to the plethora of immune structure and function research performed by immunologists to better understand the human immune system. As such, the mouse has been the most employed rodent for immunotoxicity testing. Immune system function assays employed in screening for immunotoxicity were developed in adult mice. These same immune function assays have served to help identify toxicant induced immunosuppression in the rat. 

The exact mechanism by which chemical exposures cause MCS is unknown. It is believed that a two-step process occurs. First, an initial exposure or chronic exposures interacts with a susceptible individual, leading to loss of that person s prior, natural tolerance for everyday, low-level chemicals, as well as certain foods, drugs, alcohol, and caffeine. In the second stage, symptoms are thereafter triggered by extremely low doses of previously tolerated products and exposures.2 This theory is called toxicant-induced loss of tolerance or TILT. 3... 

Elucidate nature of specific types of target organ toxicities induced by repeated exposure. 

The PBPK model development for a chemical is preceded by the definition of the problem, which in toxicology may often be related to the apparent complex nature of toxicity. Examples of such apparent complex toxic responses include nonlinearity in dose-response, sex and species differences in tissue response, differential response of tissues to chemical exposure, qualitatively and/or quantitatively difference responses for the same cumulative dose administered by different routes and scenarios, and so on. In these instances, PBPK modeling studies can be utilized to evaluate the pharmacokinetic basis of the apparent complex nature of toxicity induced by the chemical. One of the values of PBPK modeling, in fact, is that accurate description of target tissue dose often resolves behavior that appears complex at the administered dose level. 

Cannabidiol and THC reduced neurotoxicty induced by glutamate in cortical neurons (Hampson et al. 1998). This result was effective for toxicity induced at both NMDA and AMPA/kainate receptors, and was independent of cannabinoid receptor activity. The mechanism of neuroprotection appears to be by their potent antioxidant activity. They were even more protective against glutamate neurotoxicity than either ascorbate or o-tocopherol. 

Philbert MA, Gray AJ, Connors TA. 1987b. Preliminary investigations into the involvement of the intestinal microflora in CNS toxicity induced by 1,3-dinitrobenzene in male F-344 rats. Toxicol Lett 38 307-314. 

Sherer TT, Thrall KD, Bull RJ Comparison of toxicity induced by iodine and iodide in male and female rats. J Toxicol Environ Health 32 89-101, 1991... 

Moldeus P Toxicity induced by nitrogen dioxide in experimental animals and isolated cell systems. Stand J Work Environ Health 19 (S2) 28-34, 1993... 

OEl55 Onderoglu, S., S. Sozer, K. M. Erbil, R. Ortac, and F. Lermioglu. The evaluation of long-term effects of cinnamon bark and olive leaf on toxicity induced by streptozotocin administration to rats. J Pharm Pharmacol 1999 51(11) 1305-1312. 

Another aspect to be considered is the reversibility of a toxic effect. In most cases, toxicity induced by a chemical is essentially reversible. Unless damage to the affected organs has progressed too far, so as to threaten the survival of the organism, the individual will recover when the toxin is removed by excretion or inactivated by metabolism. However, in some cases the effect may outlast the presence of the toxin in the tissue. A typical example of such an effect is intoxication with organophos-phates, which bind essentially irreversibly to acetylcholine esterase. 

Sinigaglia M, Reguly ML, de Andrade HH (2004) Effect of vanillin on toxicant-induced mutation and mitotic recombination in proliferating somatic cells of Drosophila melanogaster. Environ Mol Mutagen 44 394-400... 

Goulden KJ, Dooley JM, Camfield PR, et al. Clinical valproate toxicity induced by acetylsalicylic acid. Neurology 1987 37 1392-1394. 

Mehta BR, Robinson BHB. Lithium toxicity induced by triamterene-hydrochlorothiazide. Postgrad Med J 1980 56 783-784. 

Salama AA, Shafey M. A case of severe lithium toxicity induced by combined fluoxetine and lithium carbonate [Letter]. Am J Psychiatry 1989 146 278. 

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