Cytotoxicity lactate dehydrogenase

Olbrich et al. [19] tested in vitro the cytotoxicity of the transfection agents, considering the viability of Cos-1 cell monolayers. Both the initial perturbation of cell integrity during the 4-h incubation and the influence on the cellular activity after 48 hours were assessed by measuring the release of lactate dehydrogenase and the mitochondrial conversion of the tetrazolium salt WST-1. Unmodified paraffin particles (SII-4) did not show cytotoxicity in the LDH (lactate dehydrogenase) release 2005 by CRC Press LLC... 

Figure 5. Pulmonary inflammatory response to chronic diesel exhaust exposure as measured in bronchoalveolar lavage fluid. The total amount or activity of material removed from the lung has been normalized to the weight of control lungs. Inflammatory response is indicated by influx of neutrophils (PMN). Cytotoxicity is indicated by extracellular lactate dehydrogenase (LDH). (Continued on next page.)...

Assays are frequently needed to detect marked and acute cytotoxicity that may confound the interpretation of cell-based efficacy assays. Neutral red uptake is one of the most commonly used cytotoxicity assays and is used in the regulatory phototoxicity assay on NT3 fibroblasts [13]. It has been show to be more sensitive than assays for mitochondrial reductive capacity such as the tetrazolium reductase assays, ATP depletion assays, or for cell permeabilization or mpture such as dye uptake or lactate dehydrogenase leakage. Lysosomes take up, protonate and trap neutral red when cellular ATP production is sufficient to maintain pH gradients. 

Bom et al. (2000) demonstrated that ort/20-hydroxyphenylacetaldehyde (4 mmol/L) was much more cytotoxic than coumarin (4 mmol/L) to Chinese hamster ovary cells Kj, a cell line that does not contain cytochromes P450. When both of these compounds were investigated in metabolically active hepatocytes isolated from male Sprague-Dawley rats, ort/20-hydroxyphenylacetaldehyde (0.8 mmol/L) caused a greater cytotoxic response compared with coumarin (0.8 mmol/L). 3-Hydroxycoumarin (0.8 mmol/L), not a product of coumarin epoxidation, did not cause a change in cell viability or an increase in lactate dehydrogenase activity. 

A number of other lines of evidence also suggested that there may be another mode-of-action for BTI poisoning by injection other than its known, general cytolytic activity (3,22-24). Using the appearance of cytosolic lactate dehydrogenase (LDH) in insect hemolymph post-injection as a marker for cytotoxicity (36-37), we found that dissolved BTI 6-endotoxin was a potent cytotoxin. When T. ni, however, were injected with dissolved BTI 5-endotoxin and then incubated at 28, 15, and 9°, there was an increase in the LD50 with a decrease in temperature (Figure 2) but the LDH levels at 3.5 PPM BTI were unaffected by temperature. 

Dibromo- and 1,1-dichloro-l-phenylbenzostiboles markedly increased the lactate dehydrogenase (LDH) activity leaked into the medium from vascular endothelial cells after 24 h treatment, suggesting that these four compounds have strong cytotoxicity to vascular endothelial cells, caused leakage in vascular smooth muscle cells, and destroyed the monolayer of both endothelial and smooth muscle cell layers <2005JHS333>. 

Using isolated rat hepatocytes, 1,3-dichloropropene was shown to be cytotoxic as measured by increases in phospholipid hydroperoxides and lactate dehydrogenase. 1,3-Dichloropropene also exhibited nephrotoxicity in vitro using rat renal cortical slices, where p-aminohippurate uptake was decreased. Genotoxicity of 1,3-dichloropropene was observed as increases in sister-chromatid exchange in human lymphocytes in vitro. 

N-Acetyl-B-D-glucosaminidase (N-Ac-Glu) 6 3), B-Gl ucuroni-dase (B-Glu) 4)and lactate dehydrogenase (LDH)(25lThe latter enzyme is located in the cytoplasm and is not actively secreted (as the other two enzymes are) but only set free if the cell membrane is destroyed the LDH liberated informs about viability of cell cultures or cytotoxic effects on macrophages of the substance tested. 

A primary requirement is that any substance or compoimd used as a lactate dehydrogenase inhibitor should at the same time be nontoxic for other body functions, espedally of the liver and kidneys. It may be noted in this context that most substances or compounds tend to be nonselective, that is, they may inhibit more than one enzyme. This nonselectivity produces the so-called adverse side effects. The encompassing term is cytotoxicity, or cell toxicity, indicating that the... 

The Absidia chitosans tested according to standard methods ASTM F813-83 and F619-79 with murine fibroblasts were found to be biocompatible in terms of cytotoxicity and lactate dehydrogenase activity, in agreement with Chung et al. [31]. By contrast, for solid-state fermentation, the chitosan production was higher (6.12 g/kg) but the MW was only 6.4 kDa [32]. 

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