Disease relevance of Appl1

• Pseudomonas aeruginosa AC869, a 3,5-dichlorobenzoate degrader, is a mouse pathogen and has a reported 50% lethal dose (LD50) of 1.05 x 10(7) CFU when given intranasally to C3H/HeJ mice (S.E. George, M.J. Kohan, M.I. Gilmour, M.S. Taylor, H.G. Brooks, J.P. Creason, and L.D. Claxton, Appl. Environ, Microbiol. 59:3585-3591, 1993) [1].
• H. Reitz (Toxicol. Appl. Pharmacol. 87, 185-205, 1987), who employed a PB-PK model for methylene chloride (CH2Cl2) to estimate the chronic toxicity of this material [2].
• These results in a unique murine model for hepatic iron overload further support recent in vivo studies (Khan et al., Toxicol. Appl. Pharmacol., 131, 63-72, 1995) that have associated induction of GST A4 with protection against oxidative stress-induced lipid peroxidation [3].
• [Fundam. Appl. Toxicol. 29 (1996) 40] reported that a single oral dose as low as 10 ng TCDD/kg increased the mortality of mice infected with influenza A virus [4].
• Intermittent hypoxia has been implicated in morbidities associated with sleep apnea, and may be a novel cellular signal for inflammation [J. Appl. Physiol. 90 (2001) 1986] [5].

High impact information on Appl1

• By using a specific antibody we have localized DIP13 to microtubule structures, namely basal bodies, flagellar axonemes and cytoplasmic microtubules [6].
• Expression of the DIP13 open reading frame in antisense orientation in Chlamydomonas resulted in multinucleate, multiflagellate cells, which suggests a role for this protein in ensuring proper cell division [6].
• We hypothesize from these and previous data from our laboratory (Gu XQ and Haddad GG. J Appl Physiol 91: 1245-1250, 2001) that this increased excitability is a reflection of an enhanced central nervous system maturation when exposed to low O(2) conditions in early postnatal life [7].
• A previously developed protocol (L. J. Anguish and W. C. Ghiorse, Appl. Environ. Microbiol. 63:724-733, 1997) for determining viability of oocysts in soil and sediment was used to examine further the use of oocyst permeability status as an indicator of oocyst viability in fecal material stored at 4 degrees C and in water at various temperatures [8].
• We recently reported increased ozone (O(3))-induced hyperresponsiveness to methacholine in obese mice (Shore SA, Rivera-Sanchez YM, Schwartzman IN, and Johnston RA. J Appl Physiol 95: 938-945, 2003) [9].

Biological context of Appl1

• These findings are consistent with those published for mice (MacGregor et al., Fund. Appl. Toxicol., 14, 513-522, 1990) and show that a bone marrow micronucleus test can be successfully integrated into a routine subchronic rat toxicology study [10].
• The model's foundation is a mathematical description of the physiological changes that occur during gestation (O'Flaherty et al., Toxicol. Appl. Pharmacol. 112, 245-256, 1992) [11].
• A recent study (C. R. Elcombe, M. S. Rose, and I.S. Pratt (1985), Toxicol. Appl. Pharmacol. 79, 365-376) suggested that the species difference in the hepatocarcinogenicity of TCE seen between rats and mice was due to a species difference in peroxisomal proliferation and cell proliferation [12].
• Rembaum, Appl. Polym. Symp. No. 22, 299, 1973) to produce the following biological effects: 1) bactericidal action, 2) formation of insoluble complexes with DNA and heparin, 3) neuromuscular blocking action, 4) cell aggregation and lysis, and (5) cell adhesion [13].
• The purpose of this investigation was to determine the toxicokinetics of inhaled isoprene in B6C3F1 mice and to compare the data to previously published toxicokinetic data in F344 rats (A. R. Dahl, L. S. Birnbaum, J. A. Bond, P. G. Gervasi, and R. F. Henderson, 1987. Toxicol. Appl. Pharmacol. 89, 237-248) [14].

Anatomical context of Appl1

• LPS-stimulated primary mouse macrophages produced less TNF-alpha protein and message after treatment with the herbicide propanil (Xie et al., Toxicol. Appl. Pharmacol. 145, 184-191, 1997) [15].
• Re: dioxin increases reactive oxygen production in mouse liver mitochondria (toxicol. Appl. Pharmacol.178, 15-21, 2002). To the editor [16].
• Gavage bolus doses as high as 1200 mg/kg did not cause rapid elevation of serum enzyme levels, typical of the solvation of hepatocellular membranes observed after portal vein administration of TCE (Lee et al., Toxicol. Appl. Pharmacol. 163, 000-000, 2000) [17].
• Independent of ethanol exposure, NK cell activity in nylon wool-nonadherent (NWNA) splenocytes is lower in trained than in sedentary control mice (Blank et al. J. Appl. Physiol. 72: 8-14, 1992) [18].
• In addition, glutathione (GSH) concentrations were measured in liver, lung, kidney, and testis to assess the role of the GSH depletion in the saturable metabolism previously observed in mice (Brown et al., Toxicol. Appl. Pharmacol. 136, 8-19, 1996) [19].

Associations of Appl1 with chemical compounds

• Trichloroethene (TCE) and one of its metabolites dichloroacetyl chloride (DCAC) are known to induce/accelerate autoimmune (AI) response in MRL+/+ mice as evident from anti-nuclear, anti-ssDNA, anti-cardiolipin, and DCAC-specific antibodies in the serum (Khan et al., Toxicol. Appl. Pharmacol. 134, 155-160, 1995) [20].
• DFP concentrations in mouse plasma and brain were successfully simulated after a single iv injection (B.R. Martin, 1985, Toxicol. Appl. Pharmacol. 77, 275-284) [21].
• Preconceptional exposure of male NIH Swiss mice to chromium(III) chloride resulted in increased incidence of neoplastic and non-neoplastic changes in their progeny, including lung tumors in females [Toxicol. Appl. Pharmacol. 158 (1999) 161-176] [22].
• Previously, we reported that cadmium reduced the relative abundance of the sodium-glucose cotransporter mRNA (Blumenthal et al., Toxicol. Appl. Pharmacol.149, 49-54, 1998) [23].
• Previous studies in our laboratory showed a synergistic interaction of synthetic ligands selective for the retinoid receptors RAR and RXR in regard to teratogenic effects produced in mice (M. M. Elmazar et al., 2001, TOXICOL: Appl. Pharmacol. 170, 2-9) [24].

Analytical, diagnostic and therapeutic context of Appl1

• Allele-specific expression was then analyzed by means of the previously described quantitative RT-PCR single nucleotide primer extension (SNuPE) assay (Singer-Sam et al., PCR Methods Appl. 1:160-163, 1992) [25].
• The ability of the model to predict across routes of exposure was assessed with intravenous injection data (5.6 microg/kg bw) (Li et al., 1995, Fundam. Appl. Toxicol. 27, 70-76) in female rats [26].
• (R. A. Corley, A. L. Mendrala, F. A. Smith, D. A. Staats, M. L. Gargas, R. B. Conolly, M. E. Andersen, and R. H. Reitz, 1990, Toxicol. Appl. Pharmacol. 103, 512-527) PBPK model for chloroform to reconcile the available bioassay data [27].
• Both spaceflight and skeletal unloading suppress the haematopoietic differentiation of macrophages (Sonnenfeld et al., Aviat. Space Environ. Med., 61:648-653, 1990; Armstrong et al., J. Appl. Physiol., 75:2734-2739, 1993) [28].

References