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Chloramphenicol
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
Patients sensitized to chloramphenicol may cross-react to p-nitrobenzoic acid and p-dinitrobenzene (1,4- dinitrobenzene) (32,34). Both compounds are apparently intermediates in the chloramphenicol synthesis (34).
Renal Drug-Metabolizing Enzymes in Experimental Animals and Humans
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Much of the early work relied on differences in substrate specificity to determine different isoenzymes. Today, certain model substrates are still used as markers of certain subunits, along with HPLC or fast protein liquid chromatography (FPLC) separation techniques and specific antibodies. l-Chloro-2-4-dinitrobenzene is a general substrate with good activity with all subunits except 5-5 (Table 3). Other substrates show marked specificity, but it is not absolute; for example, 1,2-dichloro-3-nitrobenzene is more active with 3-3 and 6-6 subunits, 1,2-epoxy-3 (p-nitrophenoxy) propane with the 5-5 subunit, 2-hydroxynon-2-enal with the 8-8 subunit, and A5-androstene-3,17-dione with the 1-1 subunit (Table 3).
Biochemical Methods of Studying Hepatotoxicity
Published in Robert G. Meeks, Steadman D. Harrison, Richard J. Bull, Hepatotoxicology, 2020
Prasada Rao S. Kodavanti, Harihara M. Mehendale
The method for measuring GSTase activity usually involves simple spectrophotometric assay unless there is a special interest in isoenzyme pattern. The basic principle behind spectrophotometric method is that electrophilic substrates will bind to GSH with the help of enzyme and form a colored GSH-substrate complex. This has a specific absorption maximum. Several substrates are available for GSTases; however, two substrates are widely used (l-chloro-2,4-dinitrobenzene; 1,2-dichloro-4-nitrobenzene) for spectrophotometric measurement of activity. The method described here is that of Habig et al. (1974), which uses l-chloro-2,4-dinitrobenzene as substrate.
A patent review of MAPK inhibitors (2018 – present)
Published in Expert Opinion on Therapeutic Patents, 2023
Valentin R Wydra, Raphael B Ditzinger, Nico J Seidler, Frederik W Hacker, Stefan A Laufer
B1 is a potent p38α/β-inhibitor (IC50 = 27 nM), which showed a high selectivity at a concentration of 1 µM in a panel of 94 kinases. At a concentration of 2 µM and 20 µM the compound showed a more pronounced cellular effect than SB203580 (figure 3), a representative p38α-inhibitor which was used as a reference. This cellular effect was measured by the amount of TNFα and the amount of IL-6 mRNA that was produced in THP-1 cells after stimulation with LPS [38]. In addition, the effects of B1 have been studied in cell and animal models for various diseases. It showed an antiviral effect against RSV and influenza A due to the reduction of the virus replication [45]. It also showed and antiviral effect against HBV. B1 reduced the production of the viral antigen (HBsAG) and the replication of HBV at a concentration of 5 µM [46]. In BV2 microglia cells B1 reduced LPS induced activation of p38α, as well as the production of nitric oxide, PGE2, and the proinflammatory cytokines TNFα, IL-1, and IL-6 [47]. In mice B1, reduced LPS induced neuro inflammation, β-amyloid-deposition, and the loss of spatial memory [47,48]. In a disease model for atopic dermatitis in mice B1 reduced the 1-chloro-2,4-dinitrobenzene (CDNB) induced symptoms [49]. At last B1 could reduce the allergic reaction in lungs and in the bronchoalveolar lavage in mice, in which allergic asthma was induced by ovalbumin [50].
Development of reliable quantitative structure–toxicity relationship models for toxicity prediction of benzene derivatives using semiempirical descriptors
Published in Toxicology Mechanisms and Methods, 2023
Ayushi Singh, Sunil Kumar, Archana Kapoor, Parvin Kumar, Ashwani Kumar
Because the sign of the total energy coefficient is negative in Equation (6) but positive for the molecular weight, a higher negative value of the total energy parameter will increase the toxicity of benzene derivatives. This suggests that benzene compounds with higher stability have higher toxicity. Benzene compounds with a higher molecular weight are more hazardous. Total energy and molecular weight had standardized coefficients of −0.6594 and 0.3671, respectively, indicating that total energy plays a greater role in toxicity. As shown in Table S1 and Figure S1, for 1,2-dinitrobenzene, the total energy and molecular weight are −2337.984 and 168.1086, respectively, while NB has −1578.012 and 123.1110. Because 1,2-dinitrobenzene has lower total energy and a larger molecular weight, it is more hazardous. Similarly, the total energy and molecular weight of 2-chloronitrobenzene are −1831.404 and 157.5561, respectively, whereas the total energy and molecular weight of 3,4- dichloronitrobenzene are −2084.900 and 192.0012. As a result, 3,4-dichloronitrobenzene is more toxic. The graphs for explaining Model 1 are given in Figures 1 and 2 here and Figure S2 of Supplementary Information while for Model 2 graphs are shown in Figures S3–S5 of Supplementary Information.
Nω-nitro-L-arginine, a nitric oxide synthase inhibitor, attenuates nickel-induced neurotoxicity
Published in Drug and Chemical Toxicology, 2022
Omamuyovwi M. Ijomone, Oritoke M. Aluko, Comfort O. A. Okoh, Azubuike P. Ebokaiwe
GSH-Px activity was measured according to protocols developed by Rotruck et al. (1973). The assay is performed in solution of sodium phosphate buffer, 10 mM sodium azide, 4 mM GSH, 2.5 mM H2O2, and brain homogenate. Following a 3 min incubation, 0.5 mL of 10% trichloroacetic acid (TCA) was added to solution. Thereafter, residual glutathione content was assessed by the addition of 4mL disodium hydrogen phosphate (0.3 M) solution and 1 mL of the Ellman’s (DTNB) reagent (Thermo Scientific, Waltham, MA) to the supernatant. Activity of enzyme is indicated as units/mg of protein. GST was assessed using of Habig et al. (1974) protocols, with the substrate, 1-Chloro-2,4-dinitrobenzene (CDNB). The assay was performed in a solution of 100 mmol/L phosphate buffer (pH 6.5), 30 mmol/L of CDNB, and 20 μL of brain homogenates. Enzyme activity is indicated as nmoles of CDNB/GSH conjugate generated in 1 min/mg of protein via an extinction coefficient of 9.6 L/(mmol/cm). GSH was assessed using Jollow et al. (1974) protocols. The assay was performed in a solution of 4% sulfosalicylic acid, brain homogenates, and later 4.5 ml of DTNB. Values are indicated in μg/mg protein.