Evaluation of cytotoxicity in cultured cells by enzyme leakage

Mitchell, David B.; Santone, Kenneth S.; Acosta, Daniel

doi:10.1007/bf02082861

Cited by 213 publications

(68 citation statements)

References 10 publications

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“…The increased activities of serum enzymes indicative of hepatocellular damage of silver carp in this study have been generally in agreement with previous observation in both acute and chromic toxicity studies in fish (Råbergh et al, 1991;Tencalla and Dietrich, 1997;Malbrouck et al, 2003;Li et al, 2004). It is reported that increased release of ALT into the blood is indicative of damage to the integrity of hepatocyte membranes (Mitchell et al, 1980), and the elevated AST activities are due to mitochondrial disruption as a consequence of heavy hepatitis (Schmidt and Schmidt, 1974).…”

Section: Discussionsupporting

confidence: 92%

Sequential ultrastructural and biochemical changes induced in vivo by the hepatotoxic microcystins in liver of the phytoplanktivorous silver carp Hypophthalmichthys molitrix

Xie

Li³

et al. 2007

Comparative Biochemistry and Physiology Part C: Toxicology &

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Section: Discussionsupporting

confidence: 92%

Sequential ultrastructural and biochemical changes induced in vivo by the hepatotoxic microcystins in liver of the phytoplanktivorous silver carp Hypophthalmichthys molitrix

Xie

Li³

et al. 2007

Comparative Biochemistry and Physiology Part C: Toxicology &

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“…On the contrary to most previous results, the reduced activity of ALT was observed in both fishes, while reduction in AST activity was recorded in silver carp. Increased release of ALT into the blood is indicative of damage to the integrity of hepatocyte membranes (Mitchell et al, 1980), and the elevated AST activities are due to mitochondrial disruption as a consequence of heavy hepatitis (Schmidt and Schmidt, 1974). However, we have revealed that the subcellular organs in hepatocytes of H. molitrix and A. nobilis were in good condition during the blooms (Qiu et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Plasma biochemical responses of the planktivorous filter-feeding silver carp (Hypophthalmichthys molitrix) and bighead carp (Aristichthys nobilis) to prolonged toxic cyanobacterial blooms in natural waters

Qiu

Xie

Li-wei

et al. 2009

Environmental Toxicology and Pharmacology

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“…Lactate dehydrogenase (LDH) activity was determined by a method based on the disappearance of NADH, as previously described for cells in culture (20). Total LDH activity was determined by lysing the monolayer with 0.1% Triton X-100 and determining the activity in the lysate.…”

Section: Measurement Of Lactate Dehydrogenase Releasementioning

confidence: 99%

Oxidative Injury Induces Influx-Dependent Changes in Intracellular Calcium Homeostasis

et al. 1991

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Understanding of the mechanisms of cell injury and cell death is fundamental to the understanding of both protection against and initiation ofcell injury and cell death. We subjected primary cultures of proximal tubular epithelium (PTE) from adult rats to an exogenous oxidative stress, generated by xanthine/xanthine oxidase (X/XOD), and studied its effect on the concentration of cytosolic ionized calcium ([Caz+]J by means of digital imaging fluorescence microscopy (DIFM) using a cytosolic calcium probe, fura-2. Exposure to 25 mU/ml X/XOD caused notable increases in [CaZ+], detectable within 15 sec and increasing to micromolar levels with time. Experiments with Ca2+-free medium containing ethylene glycol-bis(/3-aminoethyl ether)N,N,N',N'-tetraacetic acid (EGTA) showed that the increase of [CaZ+], was due to influx from the extracellular space. Smaller and slower increases in [CaZ+li were seen after exposure to lower concentrations of X/XOD (5 and 10 mU/ml). PTE injury and killing were assessed by measuring the release of cytosolic lactate dehydrogenase (LDH), exclusion of trypan blue, and observation of morphologic changes. Exposures to the 25 mU/ml concentration of X/XOD caused significant LDH release after 2 hr and correlated with trypan blue staining of exposed cells. Again, lesser concentrations of X/XOD resulted in a slower release of smaller amounts of LDH, and thus delayed trypan blue staining. Cytoplasmic bleb formation was seen by phase microscopy within minutes of exposure to 25 mU/ml, followed by cell rounding, retraction, and disintegration. Transmission electron microscopy revealed a progression of changes characteristic of lethal cell injury, beginning with dilatation of the endoplasmic reticulum, detachment of ribosomes, condensation of mitochondria, and chromatin clumping and terminating with mitochondria1 swelling and formation of intramitochondrial flocculent densities. These studies clearly show that notable increases of [Ca*+], precede both sub-lethal and lethal changes in rat PTE. These results indicate that interventions designed to minimize or to accelerate calcium entry could be of importance in cell preservation or cell killing, respectively, and therefore to therapeutic strategies for myocardial infarction, stroke, or shock in the former instance and for cancers in the latter.

show abstract

Evaluation of cytotoxicity in cultured cells by enzyme leakage

Cited by 213 publications

References 10 publications

Sequential ultrastructural and biochemical changes induced in vivo by the hepatotoxic microcystins in liver of the phytoplanktivorous silver carp Hypophthalmichthys molitrix

Sequential ultrastructural and biochemical changes induced in vivo by the hepatotoxic microcystins in liver of the phytoplanktivorous silver carp Hypophthalmichthys molitrix

Plasma biochemical responses of the planktivorous filter-feeding silver carp (Hypophthalmichthys molitrix) and bighead carp (Aristichthys nobilis) to prolonged toxic cyanobacterial blooms in natural waters

Oxidative Injury Induces Influx-Dependent Changes in Intracellular Calcium Homeostasis

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