The uptake of the cyanobacterial hepatotoxin microcystin by isolated rat hepatocytes

Runnegar, Maria T. C.; Gerdes, Robert; Falconer, Ian R.

doi:10.1016/0041-0101(91)90038-s

Cited by 120 publications

(72 citation statements)

References 20 publications

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“…MC can potently inhibit protein phosphatase type-1 and 2A after the toxin was transported to cytoplasm by the bile acid transporter in the cell membrane of hepatocytes and the inhibition may disturb the cellular phosphorylation balance Matsuhima et al, 1990;Eriksson et al, 1990a;Runnegar et al, 1991Runnegar et al, , 1999, caused the marked increase of ROS contents and the depletion of GSH in hepatocytes. As a result, these changes would lead to oxidant shock in hepatocytes.…”

Section: Discussionmentioning

confidence: 99%

Responses of antioxidant systems in the hepatocytes of common carp (Cyprinus carpio L.) to the toxicity of microcystin-LR

Liu

Song

et al. 2003

Toxicon

224

144

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Section: Discussionmentioning

confidence: 99%

Responses of antioxidant systems in the hepatocytes of common carp (Cyprinus carpio L.) to the toxicity of microcystin-LR

Liu

Song

et al. 2003

Toxicon

224

144

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“…The keratin phosphorylation was more sensitive to okadaic acid than to microcystin, probably relating to the fact that okadaic acid is internalized more directly by hepatocytes than microcystin, 14,23 the latter apparently requiring uptake by bile acid transporters. 24,25 The high potency of okadaic acid would suggest a type 2A protein phosphatase as the enzyme being inhibited by the toxin; the type 1 phosphatases being several orders of magnitude less sensitive to okadaic acid. 1 Naringin completely prevented the keratin overphosphorylations induced by either okadaic acid or microcystin ( Figure 1E).…”

Section: Prevention Of Toxin-induced Cytoskeletal Changes By Naringinmentioning

confidence: 99%

Prevention of toxin-induced cytoskeletal disruption and apoptotic liver cell death by the grapefruit flavonoid, naringin

2000

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The protein phosphatase-inhibitory algal toxins, okadaic acid and microcystin-LR, induced overphosphorylation of keratin and disruption of the keratin cytoskeleton in freshly isolated rat hepatocytes. In hepatocyte cultures, the toxins elicited DNA fragmentation and apoptotic cell death within 24 h. All these toxin effects could be prevented by the grapefruit flavonoid, naringin. The cytoprotective effect of naringin was apparently limited to normal hepatocytes, since the toxininduced apoptosis of hepatoma cells, rat or human, was not prevented by the flavonoid. Cell Death and Differentiation (2000) 7, 739 ± 746.

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“…It is accepted that the cellular uptake of MCLR is mediated by a bile acid carrier system present in hepatocytes (22). These low molecular weight toxins act as strong inhibitors of protein phosphatases 1 and 2A, which regulate numerous biological process, leading to an increase of protein phosphorylation in the cell (12).…”

mentioning

confidence: 99%

Influence of Microcystin-LR on the activity of membrane enzymes in rat intestinal mucosa

Moreno

Mate

Repetto

et al. 2003

J. Physiol. Biochem.

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I. M. MORENO, A. MATE, G. REPETTO, C. M. VÁZQUEZ and A. M. CAMEÁN. Influence of Microcystin-LR on the activity of membrane enzymes in ratintestinal mucosa. J. Physiol. Biochem., 59 (4), [293][294][295][296][297][298][299][300] 2003.The objective of the present study was to evaluate the effects of microcystin-LR (MCLR) on the activity of membrane enzymes from intestinal mucosa. In addition, serum chemistry and peroxidative status of both serum and intestinal homogenate were evaluated after treatment with MCLR. Wistar rats were treated with intraperitoneal injection of either 100 µg pure MCLR/Kg body weight or saline solution. A significant increase in liver weight and altered serum enzyme activities were found in MCLR-treated rats, indicating damage to the liver in these rats, as previously suggested. A higher specific activity of sucrase (1.5-fold) was observed after the administration of MCLR, whereas other intestinal apical membrane enzymes, such as lactase, maltase and alkaline phosphatase were not modified by the treatment. The specific activities of acid phosphatase and succinate dehydrogenase, markers for lysosomal and mitochondrial membranes, respectively, were also increased (32% and 60%, respectively) in treated rats. The analysis of lipid peroxidation showed that the peroxidative status was increased in both serum and intestinal mucosa from MCLRtreated rats, reflecting an excess production of oxygen free radicals induced by this cyanobacterial toxin. In conclusion, this study shows that acute exposure to MCLR affects the intestinal physiology by modifying the intestinal peroxidation status as well as the activity of membrane enzymes.

show abstract

The uptake of the cyanobacterial hepatotoxin microcystin by isolated rat hepatocytes

Cited by 120 publications

References 20 publications

Responses of antioxidant systems in the hepatocytes of common carp (Cyprinus carpio L.) to the toxicity of microcystin-LR

Responses of antioxidant systems in the hepatocytes of common carp (Cyprinus carpio L.) to the toxicity of microcystin-LR

Prevention of toxin-induced cytoskeletal disruption and apoptotic liver cell death by the grapefruit flavonoid, naringin

Influence of Microcystin-LR on the activity of membrane enzymes in rat intestinal mucosa

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