Disease relevance of Medamine

• However, administration of Carbendazim by itself did not produce lymphomas in the first generation [1].
• The role of the benomyl metabolite carbendazim in benomyl-induced testicular toxicity [2].
• Evaluation of carbendazim for gene mutations in the Salmonella/Ames plate-incorporation assay: the role of aminophenazine impurities [3].
• When given during during meiosis I, carbendazim treatment (750 or 1000 mg/kg body weight) significantly reduced the percentage of pregnant hamsters [4].
• Peri-fertilization exposure to Carbendazim (MBC; a microtubule poison) induces infertility and early pregnancy loss in hamsters [5].

High impact information on Medamine

• Depolymerisation of actin with latrunculin B did not affect the timing of Myo2 accumulation at the cell equator (although Myo2 no longer formed a ring), whereas depolymerisation of microtubules with either thiabendazole (TBZ) or methyl 2-benzimidazolecarbamate (MBC) resulted in a delay of up to 90 minutes in CAR formation [6].
• Transplacental induction of lymphomas in Swiss mice by carbendazim and sodium nitrite [1].
• Preclinical antitumor activity and pharmacokinetics of methyl-2-benzimidazolecarbamate (FB642) [7].
• Methyl-2-benzimidazolecarbamate (carbendazim, FB642) is an anticancer agent that induces apoptosis of cancer cells [7].
• Tyrosinated alpha-tubulin (52 kDa) was localized in both tubulin pools and had decreased tyrosination in the microtubule pool after carbendazim treatment [8].

Chemical compound and disease context of Medamine

• Toxicity of binary mixtures of cadmium-copper and carbendazim-copper to the nematode Caenorhabditis elegans [9].
• Here, we study the physiological mode of action of three different compounds (cadmium, carbendazim, and pentachlorobenzene) with an experimental data-based approach using whole life-cycle toxicity data from the nematode Acrobeloides nanus [10].
• Ten pesticides had sufficient laboratory data to enable the observed higher-tier effects to be compared with 5% hazardous concentrations (HC5) estimated from acute toxicity laboratory data (atrazine, carbendazim, chlorpyrifos, diazinon, dimethoate, gamma-hexachlorocy-clohexane, lambda-cyhalothrin, parathion, pentachlorophenol, and propoxur) [11].
• These results suggest that androgen- and androgen receptor-dependent mechanisms are possibly involved in carbendazim-induced toxicity [12].
• When a compound produced infertility through direct effects of testicular function (Carbendazim (MBC) and dibutyl phthalate (DBP)), then testis weight, testicular histology, and testicular sperm head counts provided sensitive indicators of toxicity [13].

Biological context of Medamine

• In order to study the mechanisms of nondisjunction at meiosis I in oocytes gonadotropin-stimulated Djungarian hamsters were treated at two stages [4.5 and 6 h post human chorionic gonadotropin (HCG)] during the preovulatory period with 1000 mg/kg Carbendazim (MBC) [14].
• An altered beta-tubulin gene that confers resistance to benomyl [whose active ingredient is 2-(methoxycarbonylamino)benzimidazole (MBC)] was isolated from a DNA library of Aspergillus flavus and used as a selectable marker for transformation [15].
• In this study, we investigated the effects of carbendazim and colchicine on microtubule polymerization status and posttranslational modifications of tubulin in freshly isolated rat seminiferous tubules [8].
• MBC caused metaphase arrest and abnormal chromosome organization following a 3-15 h treatment at a concentration of 30 microM [16].
• Excluding the negative control, water, only the fungicide carbendazim failed to induce aneuploidy in either test system [17].

Anatomical context of Medamine

• A transient dysfunction of the neuromuscular junction due to carbendazim intoxication [18].
• Long-term effects of carbendazim on the testis were induced primarily by ductal occlusions [19].
• In the immunocytochemical analysis using an antibody mMN7 that recognizes a protein delivered from the Golgi apparatus to the acrosome, spermatids exposed to carbendazim showed various abnormal immunostaining patterns in the acrosomes [20].
• Using binucleate human lymphocytes coupled with FISH, we have been able to characterize a threshold mechanism of action for two spindle inhibitors, benomyl and its active metabolite, carbendazim [21].
• Carbendazim-induced abnormal development of the acrosome during early phases of spermiogenesis in the rat testis [20].

Associations of Medamine with other chemical compounds

• Cells grown in the presence of the microtubule synthesis inhibitors nocodazole and carbendazim elaborated only a stunted rhizoid system, so we examined their ability to accumulate the two classes of compounds [22].
• A high-performance liquid chromatographic (HPLC) assay for methyl 5-hydroxy-2-benzimidazole carbamate (5-HBC) in urine was developed in order to assess the exposure of workers to the pesticide carbendazim [23].
• Selective clean-up applicable to aqueous acetone extracts for the determination of carbendazim and thiabendazole in fruits and vegetables by high-performance liquid chromatography with UV detection [24].
• Acute and long-term effects of a single dose of the fungicide carbendazim (methyl 2-benzimidazole carbamate) on the male reproductive system in the rat [19].
• With SCGE assay performed after a 1-h treatment, similar positive results were observed with chlorothalonil alone or in association with carbendazim, without any loss of cell viability [25].

Gene context of Medamine

• Benomyl and carbendazim proved negative for agonistic and antagonistic activity in reporter gene assays for the human estrogen receptor alpha and androgen receptor [26].
• The present study was performed to determine whether exposure to carbendazim induced Sertoli cell deformation [27].
• The known aneuploidogens, benomyl and its metabolite, carbendazim (methyl 2-benzimidazole carbamate (MBC)), were selected for the third in a series of ongoing projects with selected pesticides [28].
• The role of GTP Binding and microtubule-associated proteins in the inhibition of microtubule assembly by carbendazim [29].
• Carbendazim caused no signs of histological damage to the mouse testis, and the microtubule cytoskeleton was intact and identical to controls based on immunostaining with tyrosinated alpha tubulin and beta tubulin antibodies [30].

Analytical, diagnostic and therapeutic context of Medamine

• Fertility (percent fertile as indicated by pregnant females) of males in the carbendazim-treated group was depressed the first post-exposure week; 10 of the 24 treated males failed to produce a pregnant female as compared with no failures in the control group [31].
• Determination of carbendazim in blueberries by reversed-phase high-performance liquid chromatography [32].
• In contrast, carbendazim was not cytotoxic on human PBL and did not induced DNA damage using the SCGE assay either immediately after treatment or after a 24-h post-treatment incubation [25].
• Carbendazim reached the highest concentrations in stomach and small intestine by 1 h after oral administration (500 mg/kg) to tumor-bearing nude mice [33].
• Effects of a single, high dose of orally administered carbendazim (100 mg/kg) on acrosome formation in the early phases of spermiogenesis were examined by electron microscopy and immunocytochemistry up to day 7.5 post-treatment [20].

References