, 2010) The finding that BCL-XL was not capable of inhibiting ac

, 2010). The finding that BCL-XL was not capable of inhibiting acidification of lysosomes, but could inhibit their permeabilization, may indicate a lysosomal inhibition site of BCL-XL. By demonstrating that Cd causes a programmed form of cell death with a necrotic AZD6244 endpoint the present study may add to the pathobiological understanding of Cd-induced death signalling, and

the pro-inflammatory, and pro-atherosclerotic activity of Cd in vivo (Knoflach et al., 2011). This project was supported by the Austrian National Bank [project 14590 to B.M.]. The authors declare that they have no conflicts of interest. “
“Aristolochic acid (AA), a chemical found in Aristolochia and Asarum species, is present in a number of botanical products sold as “traditional medicines”, dietary supplements or weight-loss remedies. AA is a ∼1:1 mixture of two forms, aristolochic acid I (AAI) and aristolochic acid II (AAII), of which the first has higher nephrotoxicity in cellular and animal models ( Shibutani et al., 2007). AA is a rodent carcinogen and was responsible for aristolochic acid-induced nephropathy (AAN) among women under slimming regime in Belgium and China ( Arlt et al., 2002). Moreover, it is one of the possible causative agents of Balkan endemic nephropathy (BEN) ( Stefanovic et al., 2006). The Doxorubicin chemical structure major targets of AA-induced toxicity are kidneys

and urothelial tracts ( Stiborova et al., 2008). AA was reported to be among the most potent 2% of

known carcinogens and herbal remedies contaminated with Aristolochia were classified as carcinogenic to humans (Group 1) by the International Agency for Research on Cancer (IARC) ( Arlt et al., 2002 and IARC, 2002). BEN development is also closely correlated with the occurrence of ochratoxin A (OTA), one old of the mycotoxins produced by members of Aspergillus and Penicillium family ( O’Brien and Dietrich, 2005 and Pfohl-Leszkowicz and Manderville, 2007). The presence of this compound is proven for plant-derived products such as cereals, coffee and bread. Still, it was also detected in cocoa, nuts, dried vine fruits, grains as well as in wine. Pork and food products from pigs fed with contaminated grain may also be a source of OTA, what is linked to the high stability of OTA and its long half-life in blood and tissues ( International Programme on Chemical Safety, 1990). The dose of OTA may vary in food from 0.5 mg/kg in baby foods to 10 mg/kg in soluble coffee and dried vine fruits ( Coronel et al., 2010) and the tolerable intake was estimated by European Commission (1997) at 5 ng/kg body weight/day. The data from OTA presence in plasma indicated the geographical differences, being the lowest in Japanese people and the highest in Argentina. The assessed level of OTA in plasma in healthy people was 0.15 (min), 0.45 (mean) and 9.15 (max) ng OTA/ml plasma ( Coronel et al., 2010).

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