Disease relevance of Sanspor

• Enhanced renal microvascular reactivity to angiotensin II in hypertension is ameliorated by the sulfonimide analog of 11,12-epoxyeicosatrienoic acid [1].
• Captafol also induced hepatocellular carcinomas in four of 50 female rats in the 1,500 ppm group [2].
• Renal cell carcinoma was found in eight of 50 male rats treated with 1,500 ppm and in one of 50 male rats treated with 750 ppm of captafol [2].
• The incidences of renal adenomas, including micro-adenomas, and basophilic altered cell tubules were significantly higher in both sexes treated with captafol than in controls, and the increases were apparently dose-dependent except that of adenomas in females [2].
• Captafol is a common cause of dermatitis amongst workers in the timber industry [3].

High impact information on Sanspor

• Epoxyeicosatrienoic acids and their sulfonimide derivatives stimulate tyrosine phosphorylation and induce mitogenesis in renal epithelial cells [4].
• Afferent arteriolar vasodilation to the sulfonimide analog of 11, 12-epoxyeicosatrienoic acid involves protein kinase A [5].
• That the inactivation of GSTP1-1 by captan and captafol involves the formation of disulfide bonds between the four cysteinil groups of the enzymes was confirmed by the SDS-PAGE experiments on nondenaturant conditions [6].
• The IC50 values for captan and captafol were 5.8 microM and 1.5 microM, respectively [6].
• Glutathione transferase (GST, EC 2.5.1.18) P1-1 was strongly inhibited by captan and captafol in a time- and concentration-dependent manner [6].

Chemical compound and disease context of Sanspor

• The mutagenic and genotoxic potential of four pesticides viz. captan, foltaf, phosphamidon and furadan was evaluated by the Ames mutagenicity assay and their DNA damaging ability on radiation repair defective E. coli K-12 strains respectively [7].

Biological context of Sanspor

• Thirteen pesticides, aminotriazole, benomyl, captafol, captan, dalapon-Na, dichlorvos, dinobuton, dodine, ioxynil, mecoprop, neburon, picloram and tordon were tested for ability to induce (1) point mutations to 8-azaguanine resistance, (2) mitotic crossing-over, and (3) mitotic non-disjunction and haploidization in Aspergillus nidulans [8].
• Only captafol induced the SOS system in PQ35 (uvr+) [9].
• Captafol at 0.12-1.0 microgram/ml blocks the cell multiplication [10].
• 0.0002 ppm for Captafol and 0.002 ppm for Captan and Folpet, respectively, can be regarded as no observed adverse effect level (NOAEL) [11].

Anatomical context of Sanspor

• Positive results regarding increased numbers and areas of GST-P + liver cell foci were obtained in rats treated with captafol alone [12].
• The main sites of tumor formation in rats of one or both sexes (CR CD, Wistar, or F344 strains) were the kidney (Captan and captafol), uterus (captan), mammary gland and liver (captafol) [13].
• The primary sites of tumor formation with the chloroalkylthiodicarboximide fungicides in male and/or female mice (CD-1 and B6C3F1) were the gastrointestinal tract (captan, folpet, and captafol), the lymph system (folpet and captafol), and the vascular system (captafol) [13].
• Significant increases in the development of neoplastic lesions were found in the heart, spleen, forestomach, small intestine and liver of mice of both sexes treated with captafol [14].
• In V79 Chinese hamster fibroblasts higher induction of c-mitosis by captafol than by captan (22% and 15% over the control, respectively) was accompanied by a higher decrease in nonprotein sulfhydryl groups, mainly GSH (41% and 77%, respectively) [9].

Associations of Sanspor with other chemical compounds

• The positive patch test reactions were to the plants Taraxacum officinale (dandelion) and Tanacetum vulgare (tansy) and to the pesticides folpet and captafol [15].
• On the other hand, significant reduction by L-cysteine in the areas of GST-P + liver cell foci initiated by DEN and promoted by captafol was observed [12].
• The present study suggests that (a). hsp70 induction is sensitive enough to be used as a biomarker against phthalimide group of chemicals, (b). amongst the three test chemicals, Captafol is the most deleterious compound followed by Captan and Folpet, (c) [11].

Gene context of Sanspor

• Only captafol inhibited the activity of topoisomerase I (10-20% inhibition of activity in the range of 10-100microM) [16].
• In contrast, both chemicals decreased the activity of topoisomerase II already at 1microM concentration (50 and 20% inhibition of activity by captafol and captan, respectively).Genotoxicity was tested in vivo by administrating both compounds by acute (3h) and chronic feeding (48h) of 3-day-old larvae [16].
• Captafol was mutagenic in S. typhimurium strain TA102 (uvr+) and captan in strain TA104 (uvrB) [9].
• Numbers and areas of GST-P+ foci in group 1 given IQ, captafol and DES were significantly increased as compared to group 2, confirming the validity of the protocol as an initiation assay [17].
• Resolution by polarographic techniques of the ternary mixture of captan, captafol and folpet by using PLS calibration and artificial neuronal networks [18].

Analytical, diagnostic and therapeutic context of Sanspor

• Animals in group 1 were given 1500 ppm captafol in the diet, while group 2 received 1500 ppm captafol in diet as well as 1500 ppm L-cysteine in drinking water, animals in control group being given basal diet alone [12].
• Simultaneous determination of captan and captafol in apples and potatoes by thin layer chromatography and in situ fluorometry [19].

References