The cyanobacterial toxin, microcystin-LR, can induce apoptosis in a variety of cell types

The Kidney Vero-E6 Cell Line: A Suitable Model to Study the Toxicity of Microcystins

“…In our articles, we proposed that at lower MCLR concentrations, autophagy is triggered as a survival mechanism of Vero cells, in an attempt to eliminate the toxin or/and the MCLR-induced cellular damages [29,30]. Also, we reported the vacuolization of the Golgi apparatus and cytoplasm, effects also previously described in MCLR-exposed hepatocytes [17,18]. The disorganization of the microfilaments and microtubules, which is one of the most commonly described cytotoxic effects of MCLR in hepatic cells [34][35][36], was also triggered by MCLR in Vero cells [29,30].…”

“…We observed that the most sensitive methods for cytotoxicity evaluation were MTT and Neutral Red assays [26,27,29] and that the response of pure toxin and cyanobacterial extracts was quite similar with cytotoxic thresholds within 22-50 µM of MCLR ( Table 1). The MCLR-induced loss of Vero-E6 viability was attributed to apoptosis and necrosis [29,30] as widely described for various cell types in vitro and in vivo [18,31,32].…”

“…This was due to the observation that, comparing with primary cell lines, high amounts of MCs were required to elicit toxicity in permanent cell lines [17,18,19]. A proposed explanation was the fact that established cell lines lose their OATPs, which render them unable to uptake the toxin [19,20].…”

Toxicity of microcystins in the isolated hepatocytes of common carp (Cyprinus carpio L.)

“…In this study, all these cytological and biochemistry changes described as above were detected in carp hepatocytes exposed to 10 and 100 mg L À1 of microcystins for 24 h. A similar result was obtained by Pichardo et al (2005) in the microcystin-LR-treated fish cell line PLHC-1. This result was also consistent with the observation previously in rat hepatocytes (Eriksson et al, 1989;Ding et al, 1998) or cell lines of mammal (McDermott et al, 1998;Mankiewicz et al, 2001) and fish (Li et al, 2001a(Li et al, ,b, 2003. On the other hand, the mechanisms of microcystin-induced apoptosis and hepatotoxicity have not been fully elucidated until now (Ding et al, 2000).…”

Mitochondria a key role in microcystin‐LR kidney intoxication

“…Microcystin-treated hepatocytes and other types of cells have typical apoptotic morphology, including chromatin condensation, cell shrinkage and membrane blebbing. A caspase-dependent mechanism should be involved in MC toxicity, since caspase inhibitors could retard the execution (McDermott et al, 1998;Fladmark et al, 1999). However, the exact mechanisms underlying the suggested apoptosis-induced potential are still unknown.…”