Early Cretaceous adakitic granites and mineralization of the Yili porphyry Mo deposit in the Great Xing’an Range: implications for the geodynamic evolution of northeastern China

<div><p>The Yili porphyry-type molybdenum deposit is located in the Northeastern Inner Mongolia Autonomous Region in China. Mineralization occurs mainly as veins, lenses, and layers within the host porphyry. In order to better understand the link between mineralization and host igneous rocks, we studied samples from underground workings. We report new Sensitive High Resolution Ion Microprobe II (SHRIMP II) zircon U–Pb and Re–Os molybdenite ages and geochemical data from the Yili granitoids. Five molybdenite samples yield a Re–Os isochron weighted mean age of 131.1 ± 3.4 Ma, while two Early Cretaceous adakitic porphyry granite samples yielded crystallization ages of 128.1 ± 1.6 Ma and 129.0 ± 3.5 Ma. The U–Pb and Re–Os ages are analytically indistinguishable, suggesting that mineralization was genetically related to Early Cretaceous magmatism in northeastern China. δ³⁴S_V-CDT values of the sulphide vary from 0.3‰ to 3.8‰. We obtained two weighted mean U–Pb zircon ages of 287.7 ± 1.8 Ma for early Permian fine-grained granite and 349.8 ± 2.3 Ma for Early Carboniferous monzogranite in Yili area, respectively. A synthesis of geochronological and geological data reveals that porphyry emplacement and Mo mineralization in the Yili deposit occurred at the same time as Early Cretaceous lithospheric thinning, which was caused by the delamination and subsequent upwelling of the asthenosphere under the intra-continental extension in northeastern China.</p></div

Intracellular oxidative fatty acid content analysis.

<p>Cells were collected, treated with trichloroacetic acid/TBARS reagent and incubated at 95°C for 60 min. The supernatants were analyzed, and the values are expressed as percentage of control values. The data are expressed as the means±S.D. (<i>n</i> = 6). * indicates a comparison with the blank control group (p<0.05).</p

iPLA2 expression is downregulated in t-BHP-induced apoptosis.

<p>Figure A, Western blot analysis of iPLA2 expression during t-BHP-induced apoptosis. The cells were first treated with or without Exendin-4 and then with t-BHP (200 µM for 24 hours) or H₂O₂ (100 µM for 12 hours) for different intervention times. The cells were then collected, and cell lysates were prepared and analyzed for iPLA2 and actin. B, the group gray comparison. Data are expressed as the means±S.D. (<i>n</i> = 6). a, b, c, d, e and f indicate group comparisons (p<0.05).</p

Exendin-4 prevents apoptosis induced by t-BHP.

<p>A, FACS analysis of apoptosis. Min6 cells were divided into four groups: control, t-BHP (200 µM for 24 hours), Exendin-4 (100 µM for 24 hours) and Exendin-4 (100 µM for 48 hours). Before being treated with t-BHP, the cells were treated with Exendin-4 for 24 or 48 hours). The cells were collected and stained with Annexin V and PI and analyzed by FACS. Figure B presents a summary of the results and includes a comparison of the apoptosis percentages of early-stage and late-stage. The data are expressed as the means±S.D. (<i>n</i> = 6). a, b, c and d indicate the blank control, t-BHP (200 µM for 24 hours), Exendin-4 (100 µM for 24 hours) and group comparisons with the Exendin-4 (100 µM for 48 hours) group (<i>p</i><0.05).</p

Exendin-4 reduced H₂O₂-induced Min6 cell DNA fragmentation.

<p>A, Apoptotic DNA ladder analysis. fter t-BHP (200 µM for 24 hours, as in Figure A2) and H₂O₂ (100 µM for 24 hours, as in Figure A4) treatment, the DNA was purified using an apoptosis DNA ladder kit and analyzed on agarose gel. Figures A3 and A5 represent Exendin-4 groups that were treated with t-BHP or H₂O₂ after treatment with Exendin-4 100 µM for 48 hours. Figure B is a summary of the results and includes the gray comparison among the control group, the H₂O₂ (100 µM for 24 hours) group and the Exendin-4 group. The data are expressed as the means±S.D. (<i>n</i> = 6). a, b and c indicate the respective comparisons (<i>p</i><0.05).</p

Exendin-4 reduces t-BHP-induced ROS production.

<p>Cells were treated with or without Exendin-4 and then with t-BHP for different intervention times, collected, stained with 2 µM HE and analyzed with an absorbance microplate reader. Values are expressed as percentages of total cell counts. The data are expressed as the means±S.D. (<i>n = </i>6). a, b, c, d and e indicate the t-BHP groups and Exendin-4 groups at different intervention times (<i>p</i><0.05).</p

Determination of the apoptosis rate in 1

<p>A, FACS analysis of apoptosis. The different concentrations of t-BHP were allowed to react for 1 hour to induce early (Annexin V-positive and PI-negative) and late apoptosis (Annexin V- and PI-positive) in Min6 cells, and then, FACS analysis was performed. Figure B summarizes the results and includes a comparison of the different t-BHP concentrations and Min6 cell apoptosis percentages of early-stage and late-stage. The data are expressed as the means±S.D (<i>n = </i>6). a, b, c and d show comparisons between the blank control and different concentrations of t-BHP (<i>p</i><0.05).</p

Exendin-4 reduces the Min6 cell apoptosis factor caspase 3 activity.

<p>This figure presents a comparison of the caspase 3 activity in the t-BHP group and the Exendin-4 group. Caspase 3 activity was determined with a caspase 3 assay kit. The data are expressed as the means±S.D. (<i>n</i> = 6). a, b, c, d, e and f indicate comparisons of the two groups (<i>p</i><0.05).</p

Exendin-4 prevents the loss of mitochondrial membrane potentials.

<p>An absorbance microplate reader was used to analyze the loss of mitochondrial membrane potentials. The figure shows the time course of the t-BHP-induced loss of mitochondrial membrane potential. The data are expressed as the means±S.D. (<i>n = </i>6). a, b, c, d, e and f indicate the t-BHP groups and Exendin-4 groups at different intervention times (<i>p</i><0.05).</p

Determination of the apoptosis rate in 24

<p>A, FACS analysis of apoptosis. The different concentrations of t-BHP were allowed to react for 24 hour to induce early (Annexin V-positive and PI-negative) and late apoptosis (Annexin V- and PI-positive) in Min6 cells, and then, FACS analysis was performed. Figure B summarizes the results and includes a comparison of the different t-BHP concentrations and Min6 cell apoptosis percentages of early-stage and late-stage. The data are expressed as the means±S.D (<i>n = </i>6). a, b, c, d, e and f show comparisons between the blank control and different concentrations of t-BHP (<i>p</i><0.05).</p