Protective effect of boric acid on lead- and cadmium-induced genotoxicity in V79 cells.

The toxic heavy metals cadmium (Cd) and lead (Pb) are important environmental pollutants which can cause serious damage to human health. As the metal ions (Cd(2+) and Pb(2+)) accumulate in the organism, there is special concern regarding chronic toxicity and damage to the genetic material. Metal-induced genotoxicity has been attributed to indirect mechanisms, such as induction of oxidative stress and interference with DNA repair.

Toxicity of the mycotoxin citrinin and its metabolite dihydrocitrinone and of mixtures of citrinin and ochratoxin A in vitro.

Citrinin (CIT) and ochratoxin A (OTA) are mycotoxins produced by several species of the genera Aspergillus, Penicillium and Monascus. Both can be present as contaminants in various food commodities and in animal feed. The occurrence and toxicity of OTA and human exposure have been intensively studied, but for CIT such data are scarce by comparison.

Cytotoxic potency of mycotoxins in cultures of V79 lung fibroblast cells.

In addition to dietary mycotoxin intake, exposure by inhalation is possible and may result in local effects in the lung. As a first approach to assess the potential local impact of inhaled mycotoxins, the cytotoxicity of 14 different mycotoxins was determined in V79 cell cultures, which served as an in vitro surrogate for lung cells. Cell viability was measured by the neutral red (NR) uptake assay after 48 h of exposure to graded concentrations of structurally diverse compounds: beauvericin, citrinin, enniatin B, moniliformin, ergocornine, ergotamine, fumonisin B1, ochratoxin A, patulin, the trichothecenes deoxynivalenol, HT-2, and T-2 toxin, and zearalenone, and α-zearalenol.

N-Acetylation of p-aminobenzoic acid and p-phenylenediamine in primary porcine urinary bladder epithelial cells and in the human urothelial cell line 5637.

N-Acetyltransferases (NAT) are important enzymes in the metabolism of certain carcinogenic arylamines, as N-acetylation decreases or prevents their bioactivation via N-hydroxylation. To study such processes in the bladder, cell culture models may be used, but metabolic competence needs to be characterized. This study focused on the N-acetylation capacity of two urothelial cell systems, using p-aminobenzoic acid (PABA) and the hair dye precursor p-phenylenediamine (PPD), two well-known substrates of the enzyme NAT1.

Effects of cigarette smoke condensate on primary urothelial cells in vitro.

Cigarette smoking is a risk factor for bladder cancer. Since urothelial cells express phase I and II enzymes these cells are able to metabolize precarcinogens into DNA reactive intermediates. Cigarette smoke is a complex mixture containing at least 80 known carcinogens.

The Fusarium toxin enniatin B exerts no genotoxic activity, but pronounced cytotoxicity in vitro.

Enniatin B, a fungal metabolite produced by various Fusarium strains, is a frequent contaminant in cereals used for human foods and animal feeds, but, so far very limited data are available on its toxicity. The aim of this study was to investigate the effects of enniatin B in a battery of short-term tests to evaluate its genotoxic potential. In Salmonella typhimurium assays (Ames assay) with the strains TA 98, TA 100, TA 102, and TA 104, both in the presence and absence of an external metabolizing enzyme system (rat liver S9), no mutagenicity was detected up to toxic levels (100 microM) of enniatin B.

The emerging Fusarium toxin enniatin B: in-vitro studies on its genotoxic potential and cytotoxicity in V79 cells in relation to other mycotoxins.

The Fusarium metabolite enniatin B is now recognized as a frequent contaminant of grains used for human foods and animal feeds. Yet, so far very limited data are available on its toxicity and that of other emerging Fusarium mycotoxins (Jestoi M, 2008, Crit Rev Food Sci Nutr 48:21-49). Thus, the mutagenic/genotoxic potential of enniatin B was investigated in a battery of short-term tests, and its cytotoxicity compared with that of several other mycotoxins.

Synergism of aromatic amines and benzo[a]pyrene in induction of Ah receptor-dependent genes.

Aromatic amines have been shown to cause bladder cancer. However, epithelial cells of the urinary bladder, cells of origin of bladder cancer, may be exposed to numerous substances besides aromatic amines. In the present study, we analysed possible interactions between the aromatic amines 4-aminobiphenyl (4-ABP) as well as 2-naphthylamine (2-NA) and the polycyclic aromatic hydrocarbon benzo[a]pyrene (B[a]P).

Miniaturization of primary porcine urinary bladder epithelial cell cultures and application for gene expression studies after exposure to benzo[a]pyrene.

Benzo[a]pyrene (BaP) is an environmental pollutant used as a key marker substance for polycyclic aromatic hydrocarbons (PAHs). PAHs are believed to play a prominent role in the development of bladder cancer. A test system based on primary porcine urinary bladder epithelial cells (PUBEC) has been utilized as an in vitro model for urinary bladder epithelium.

The effect of benzo(a)pyrene on porcine urinary bladder epithelial cells analyzed for the expression of selected genes and cellular toxicological endpoints.

Consumption of tobacco products is the most relevant risk factor for the development of bladder cancer beside occupational contributions. In order to investigate mechanisms of tobacco smoke components in bladder carcinogenesis we have introduced a primary epithelial cell culture system derived from porcine urinary bladder as a suitable representative for the corresponding human tissue under physiological conditions. Two independent readouts were selected as markers for genotoxic events.