Antigenotoxic Studies of Different Substances to Reduce the DNA Damage Induced by Aflatoxin B1 and Ochratoxin A

Mycotoxins are produced mainly by the mycelial structure of filamentous fungi, or more specifically, molds. These secondary metabolites are synthesized during the end of the exponential growth phase and appear to have no biochemical significance in fungal growth and development. The contamination of foods and feeds with mycotoxins is a significant problem for the adverse effects on humans, animals, and crops that result in illnesses and economic losses. The toxic effect of the ingestion of mycotoxins in humans and animals depends on a number of factors including intake levels, duration of exposure, toxin species, mechanisms of action, metabolism, and defense mechanisms. In general, the consumption of contaminated food and feed with mycotoxin induces to neurotoxic, immunosuppressive, teratogenic, mutagenic, and carcinogenic effect in humans and/or animals. The most significant mycotoxins in terms of public health and agronomic perspective include the aflatoxins, ochratoxin A (OTA), trichothecenes, fumonisins, patulin, and the ergot alkaloids. Due to the detrimental effects of these mycotoxins, several strategies have been developed in order to reduce the risk of exposure. These include the degradation, destruction, inactivation or removal of mycotoxins through chemical, physical and biological methods. However, the results obtained with these methods have not been optimal, because they may change the organoleptic characteristics and nutritional values of food. Another alternative strategy to prevent or reduce the toxic effects of mycotoxins is by applying antimutagenic agents. These substances act according to several extra- or intracellular mechanisms, their main goal being to avoid the interaction of mycotoxins with DNA; as a consequence of their action, these agents would inhibit mutagenesis and carcinogenesis. This article reviews the main strategies used to control AFB1 and ochratoxin A and contains an analysis of some antigenotoxic substances that reduce the DNA damage caused by these mycotoxins

The Finding of New In Vivo Metabolite Triptorelin (5-10) in Human Urine Using Liquid Chromatography Coupled with Ion Trap/Time-of-Flight Mass Spectrometry with Dimethyl Sulfoxide Additives in the Mobile Phase

Triptorelin and leuprorelin are synthetic gonadotrophin-releasing hormones (GnRH) that are on the World Anti-Doping Agency (WADA) list of prohibited substances. To investigate the possible in vivo metabolites of triptorelin and leuprorelin in humans compared to previously reported in vitro metabolites, excreted urine from five patients treated with either triptorelin or leuprorelin was analyzed by liquid chromatography coupled with ion trap/time-of-flight mass spectrometry (LC/MS-IT-TOF). The addition of dimethyl sulfoxide (DMSO) to the mobile phase was found to enhance the detection sensitivity of certain GnRH analogs. The method was validated, and the limit of detection (LOD) was found at 0.02−0.08 ng/mL. Using this method, a novel new metabolite of triptorelin was discovered in the urine of all subjects up to 1 month after triptorelin administration, but it was not observed in the urine of subjects before drug administration. The limit of detection was estimated to be 0.05 ng/mL. The structure of the metabolite, triptorelin (5-10), is proposed from bottom-up mass spectrometry analysis. The discovery of in vivo triptorelin (5-10) can possibly be used as supporting evidence of triptorelin misuse in athletes

Chemistry and crystal structures of some constituents of Zingiber cassumunar

The novel aromatic compounds cis-3-(2',4',5'-trimethoxyphenyl)-4-[(E)-2''',4''',5'''-trimethoxy-styryl]cyclohex-1-ene(1), cis-3-(3',4'-dimethoxyphenyl)-4-[(E)-3''',4'''-dimethoxystyryl]cyclohex-1-ene (2), a substance assigned the tentative structure cis-3-(3',4'-dimethoxyphenyl)-4-[(E)-2''',4''',5'''- trimethoxystyryl]cyclohex-1-ene (3),(E)-4-(3',4'-dimethoxypheny1)but-3-en-1-ol (5), (E)-4-(3',4'-dimethoxypheny1)but-3-en-1-yl acetate (6), and 8-(3',4'-dimethoxyphenyl)-2-methoxynaphtho-1,4- quinone (7) have been isolated from the rhizomes of Zingiber cassurnunav Roxb. (Zingiberaceae). The crystal structures of the cyclohexene derivative (1) and the quinone (7) have been determined from X-ray diffractometer data at 295 K and refined by block diagonal least squares to residuals of 0.046 (2099 'observed' reflections) and 0.093 (1246), respectively. Crystals of compound (1) are triclinic, P1, a 18.027(12), b 10.037(9), c 6.530(5) α, 84.22 (7), β 81.87 (6), γ 85.72 (6)º, Z 2. Crystals of the quinone (7) are monoclinic, P21/a, a 22.89 (1), b 8.022 (5), c 8.458 (5) Å, β 91.98 (5)º, Z 4. Although the latter crystal structure determination is imprecise, due largely to the very small size of the crystal available, the solution is unambiguous