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        Multiple Chemical Sensitivity in Chemical Laboratory Workers

        Juan Pérez-Crespo,Rafael Lobato-Cañón,Ángel Solanes-Puchol 한국산업안전보건공단 산업안전보건연구원 2018 Safety and health at work Vol.9 No.4

        Background: Multiple Chemical Sensitivity (MCS) is an acquired disease which etiology remains unknown. It is characterized by the development of sensitivity to certain chemical products. Most of the hypotheses formulated to explain the syndrome associate it to a previous exposition to some kind of volatile chemical. University researchers in chemical laboratories suffer a phenomenon of multiexposition to chemical agents at low concentration during long periods of time although in an irregular form. Many of these chemical agents have similar properties to those suspicious of causing MCS. This article studies the prevalence of MCS in laboratory researchers. Methods: The study group is university researchers in chemical laboratories. The control group was obtained from administrative personnel who work in the same universities and therefore, are not exposed to chemical products from the laboratories, but have the same exposition to the rest of environmental polluting agents from the area and from the buildings of the university. In this study, it is used the Quick Environmental Exposure and Sensitivity Inventory (QEESI) (sensitivity of 92%/specificity of 95%). Results: The results showed that the prevalence of MCS for the university researchers is not related to exposition by inhalation to multiple chemical agents, at low concentration. Conclusions: The results disagree with one of the main etiological hypotheses of MCS, which is based on the existence of hypersensitive people, who presents a response after prolonged expositions to very low concentrations during a long period of time.

      • Autophagic flux is required for the synthesis of triacylglycerols and ribosomal protein turnover in <i>Chlamydomonas</i>

        Couso, Inmaculada,Pé,rez-Pé,rez, Marí,a Esther,Martí,nez-Force, Enrique,Kim, Hee-Sik,He, Yonghua,Umen, James G,Crespo, José,L Oxford University Press 2018 Journal of experimental botany Vol.69 No.6

        <▼1><P>Inhibition of autophagic flux prevented the synthesis of triacylglycerols, formation of lipid bodies, and degradation of ribosomal proteins RPS6 and RPL37 in nitrogen- or phosphate-starved <I>Chlamydomonas</I> cells.</P></▼1><▼2><P><B>Abstract</B></P><P>Autophagy is an intracellular catabolic process that allows cells to recycle unneeded or damaged material to maintain cellular homeostasis. This highly dynamic process is characterized by the formation of double-membrane vesicles called autophagosomes, which engulf and deliver the cargo to the vacuole. Flow of material through the autophagy pathway and its degradation in the vacuole is known as autophagic flux, and reflects the autophagic degradation activity. A number of assays have been developed to determine autophagic flux in yeasts, mammals, and plants, but it has not been examined yet in algae. Here we analyzed autophagic flux in the model green alga <I>Chlamydomonas reinhardtii</I>. By monitoring specific autophagy markers such as ATG8 lipidation and using immunofluorescence and electron microscopy techniques, we show that concanamycin A, a vacuolar ATPase inhibitor, blocks autophagic flux in <I>Chlamydomonas</I>. Our results revealed that vacuolar lytic function is needed for the synthesis of triacylglycerols and the formation of lipid bodies in nitrogen- or phosphate-starved cells. Moreover, we found that concanamycin A treatment prevented the degradation of ribosomal proteins RPS6 and RPL37 under nitrogen or phosphate deprivation. These results indicate that autophagy might play an important role in the regulation of lipid metabolism and the recycling of ribosomal proteins under nutrient limitation in <I>Chlamydomonas</I>.</P></▼2>

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