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Articles by M. A Santos
Total Records ( 2 ) for M. A Santos
  S Guilherme , I Gaivao , M. A Santos and M. Pacheco
 

The glyphosate-based herbicide, Roundup®, is among the most used pesticides worldwide. Due to its extensive use, it has been widely detected in aquatic ecosystems representing a potential threat to non-target organisms, including fish. Despite the negative impact of this commercial formulation in fish, as described in literature, the scarcity of studies assessing its genotoxicity and underlying mechanisms is evident. Therefore, as a novel approach, this study evaluated the genotoxic potential of Roundup® to blood cells of the European eel (Anguilla anguilla) following short-term (1 and 3 days) exposure to environmentally realistic concentrations (58 and 116 µg/l), addressing also the possible association with oxidative stress. Thus, comet and erythrocytic nuclear abnormalities (ENAs) assays were adopted, as genotoxic end points, reflecting different types of genetic damage. The pro-oxidant state was assessed through enzymatic (catalase, glutathione-S-transferase, glutathione peroxidase and glutathione reductase) and non-enzymatic (total glutathione content) antioxidants, as well as by lipid peroxidation (LPO) measurements. The Roundup® potential to induce DNA strand breaks for both concentrations was demonstrated by the comet assay. The induction of chromosome breakage and/or segregational abnormalities was also demonstrated through the ENA assay, though only after 3-day exposure to both tested concentrations. In addition, the two genotoxic indicators were positively correlated. Antioxidant defences were unresponsive to Roundup®. LPO levels increased only for the high concentration after the first day of exposure, indicating that oxidative stress caused by this agrochemical in blood was not severe. Overall results suggested that both DNA damaging effects induced by Roundup® are not directly related with an increased pro-oxidant state. Moreover, it was demonstrated that environmentally relevant concentrations of Roundup® can pose a health risk for fish populations.

  M. A Santos , M. S. Y Huen , M Jankovic , H. T Chen , A. J Lopez Contreras , I. A Klein , N Wong , J. L. R Barbancho , O Fernandez Capetillo , M. C Nussenzweig , J Chen and A. Nussenzweig
 

53BP1 is a well-known mediator of the cellular response to DNA damage. Two alternative mechanisms have been proposed to explain 53BP1’s interaction with DNA double-strand breaks (DSBs), one by binding to methylated histones and the other via an RNF8 E3 ligase–dependent ubiquitylation pathway. The formation of RNF8 and 53BP1 irradiation-induced foci are both dependent on histone H2AX. To evaluate the contribution of the RNF8-dependent pathway to 53BP1 function, we generated RNF8 knockout mice. We report that RNF8 deficiency results in defective class switch recombination (CSR) and accumulation of unresolved immunoglobulin heavy chain–associated DSBs. The CSR DSB repair defect is milder than that observed in the absence of 53BP1 but similar to that found in H2AX–/– mice. Moreover, similar to H2AX but different from 53BP1 deficiency, RNF8–/– males are sterile, and this is associated with defective ubiquitylation of the XY chromatin. Combined loss of H2AX and RNF8 does not cause further impairment in CSR, demonstrating that the two genes function epistatically. Importantly, although 53BP1 foci formation is RNF8 dependent, its binding to chromatin is preserved in the absence of RNF8. This suggests a two-step mechanism for 53BP1 association with chromatin in which constitutive loading is dependent on interactions with methylated histones, whereas DNA damage–inducible RNF8-dependent ubiquitylation allows its accumulation at damaged chromatin.

 
 
 
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