Disease relevance of Eparen

• Yeasts as a model for assessing the toxicity of the fungicides Penconazol, Cymoxanil and Dichlofluanid [1].
• Allergic contact dermatitis from dichlofluanid [2].
• Euparen Multi was administered by rumen sonde to group of Merino sheep (seven sheep/group) at 93 mg/kg body weight (1/20 LD50) daily for 28 days to assess its genotoxic effects [3].
• Chromosomal aberrations and frequency of micronuclei in sheep subchronically exposed to the fungicide Euparen Multi (tolylfluanid) [3].

High impact information on Eparen

• Chlorothalonil, dichlofluanid and Sea nine 211 were employed as model compounds to asses the extraction procedure and were determined by gas chromatography with electron capture detection [4].
• Seven different endpoints for detection of genotoxicity have been used to demonstrate the DNA-altering properties of Dichlofluanid, a fungicide commonly used in viticulture pest control [5].
• We analyzed chromosome aberrations, micronucleus frequency, mitotic index (MI), and nuclear division index (NDI) in peripheral lymphocytes of sheep subchronically exposed to the fungicide Euparen Multi (containing 50% tolylfluanid) [3].
• Thus, our results suggest that exposure to Euparen Multi may cause genome damage in somatic cells [3].
• As expected, given its known high hydrolytic degradation rate, no detectable concentrations of dichlofluanid were measured in any of the seawater samples [6].

Chemical compound and disease context of Eparen

• Presence of MTBE increased the toxicity of Dichlofluanid by 30% when measured with the D. magna assay [7].

Biological context of Eparen

• Significant cytotoxicity occurred after 20 min (captan), 30 min (dichlofluanid) and 60 min (chlorothalonil) of incubation and lipid peroxidation was induced prior to cytotoxicity [8].
• Cell viability was considerably decreased by incubation with chlorobenzilate, edifenphos, dichlofluanid, and chinomethionat at 10(-3) M, and in these cases, depletion of cellular adenosine 5'-triphosphate (ATP) contents proceeded to cell death [9].
• The rate of decrease of dichlofluanid residues on the leaves of strawberry is proceeding according to the first-order reaction kinetics in the initial 21 days [10].
• On the basis of IC50 values the cytotoxic effect was: dichlofluanid (IC50 = 10(-3.94) M) > tolylfluanid (IC50 = 10(-3.69) M) > endosulfan (IC50 = 10(-3.24) M) > triallate (IC50 = 10(-3.12) M) > simazine (IC50 = 10(-1.78) M) [11].

Anatomical context of Eparen

• Oxidative damages in isolated rat hepatocytes treated with the organochlorine fungicides captan, dichlofluanid and chlorothalonil [8].
• Three of the pesticides tested suppressed both, the metabolic activity of phagocytes and mitogenic activation of lymphocytes (dichlofluanid, endosulfan and simazine) [12].
• The significant cytotoxic effect (the decrease of spontaneous migration of leukocytes) was registered for bentazone, dichlofluanid, endosulfan and MCPA (10(-1) M); chloridazone (10(-1) M-10(-2) M) and triallate (10(-1)-10(-5) M) [12].

Associations of Eparen with other chemical compounds

• When present as antifouling paint particles, an increased half-life of 9.9 days for SeaNine 211 and 1.4 days was calculated for dichlofluanid, no significant degradation was observed for diuron [13].
• Monitoring of the booster biocide dichlofluanid in water and marine sediment of Greek marinas [6].
• In a separate experiment, in which marine sediment was spiked with artificial paint particles containing dichlofluanid and then analysed according to the validated method, it was demonstrated that if there is any dichlofluanid originating from paint particles, this would be determined as DMSA [6].

Analytical, diagnostic and therapeutic context of Eparen

• In this study pesticides with different chemical structures (dichlofluanid, endosulfan, simazine, tolylfluanid and triallate) were examined for their potential cytotoxic effect on proliferative activity of cell cultures of mammalian origin [11].

References