Parkinson’s-disease (PD) is an incurable, age-related neurodegenerative disease, and its global prevalence of disability and death has increased exponentially. Although motor symptoms are the characteristic manifestations of PD, the clinical spectrum also contains a wide variety of non-motor symptoms, which are the main cause of disability and determinants of the decrease in a patient’s quality of life. Noteworthy in this regard is the stress on the cardiac system that is often observed in the course of PD; however, its effects have not yet been adequately researched. Here, an untargeted metabolomics approach was used to assess changes in cardiac metabolism in the 6-hydroxydopamine model of PD. Beta-sitosterol, campesterol, cholesterol, monoacylglycerol, α-tocopherol, stearic acid, beta-glycerophosphoric acid, o-phosphoethanolamine, myo-inositol-1-phosphate, alanine, valine and allothreonine are the metabolites that significantly discriminate parkinsonian rats from sham counterparts. Upon analysis of the metabolic pathways with the aim of uncovering the main biological pathways involved in concentration patterns of cardiac metabolites, the biosynthesis of both phosphatidylethanolamine and phosphatidylcholine, the glucose-alanine cycle, glutathione metabolism and plasmalogen synthesis most adequately differentiated sham and parkinsonian rats. Our results reveal that both lipid and energy metabolism are particularly involved in changes in cardiac metabolism in PD. These results provide insight into cardiac metabolic signatures in PD and indicate potential targets for further investigation.

Parkinson’s-disease (PD) is an incurable age-related neurodegenerative disease and its global prevalence of disability and death has increased exponentially. Although motor symptoms are the characteristic manifestations of PD, the clinical spectrum also contains a wide variety of non-motor symptoms, which are the main cause of disability and determinants of the decrease in a patient's quality of life. Noteworthy in this regard is the stress on the cardiac system that is often observed in the course of PD, however its effects have not yet been adequately researched. Here, an untargeted metabolomics approach was used to assess changes in cardiac metabolism in the 6-hydroxydopamine model of PD. Beta-sitosterol, campesterol, cholesterol, monoacylglycerol, α-tocopherol, stearic acid, beta-glycerophosphoric acid, o-phosphoethanolamine, myo-inositol-1-phosphate, alanine, valine and allothreonine, are the metabolites that significantly discriminate Parkinsonian rats from sham counterparts. Upon analysis of the metabolic pathways with the aim of uncovering the main biological pathways involved in concentration patterns of cardiac metabolites, biosynthesis of both phosphatidylethanolamine and phosphatidylcholine, glucose-alanine cycle, the glutathione metabolism and plasmalogen synthesis most adequately differentiated sham and Parkinsonian rats. Our results reveal that both lipid and energy metabolism are particularly involved in changes in cardiac metabolism in PD. These results provide insight into cardiac metabolic signatures in PD and indicate potential targets for further investigation.

We evaluated the effects of different concentrations (0, 10‐8 M and 10‐7M) of progesterone (P4), testosterone (T) and estradiol (E2) on the osteoblast viability in vitro. Osteoblast lineages (OSTEO‐1) were cultured in 96‐well plates in DMEM medium a density of 5 x 103 cells/100 μL medium, with or without 10% fetal bovine serum (FBS). Cells were maintained at 37 ºC, with 5% CO2, for up to 48 hours. Cell viability was analyzed by MTT tetrazolium assay. The cells cultured with 10% FBS were more viable than those cultured without FBS. When all hormones were put together, the cell viability was reduced at the 10‐7M concentrations compared with the control and 10‐8 M. The viability of cells cultured without FBS was a) stimulated by E2 (10‐7 M and 10‐8 M (0.1048 ± 0.0227 and 0.1069 ± 0.0124, respectively)) compared with the control group (0.0566 ± 0.008); b) stimulated by P4 (10‐7 M (0.1088 ± 0.0124)) compared with the control group (0.0566 ± 0.008) and 10‐8 M (0.0924 ± 0.022); and c) stimulated by both concentrations of T (10‐7 M (0.0908 ± 0.0153) and 10‐8 M (0.0924 ± 0.0022)) compared with the control group (0.0566 ± 0.008). Our results demonstrated that FBS stimulated osteoblast viability, and P4 (10‐7 M), and both concentrations of T and E2 stimulated the viability of the cells cultured without FBS, suggesting that these steroid hormones may be important at the onset of osteoblast cells viability in vitro for up to 48 hours.

We evaluated the effects of different concentrations (0, 10‐8 M and 10‐7M) of progesterone (P4), testosterone (T) and estradiol (E2) on the osteoblast viability in vitro. Osteoblast lineages (OSTEO‐1) were cultured in 96‐well plates in DMEM medium a density of 5 x 103 cells/100 μL medium, with or without 10% fetal bovine serum (FBS). Cells were maintained at 37 ºC, with 5% CO2, for up to 48 hours. Cell viability was analyzed by MTT tetrazolium assay. The cells cultured with 10% FBS were more viable than those cultured without FBS. When all hormones were put together, the cell viability was reduced at the 10‐7M concentrations compared with the control and 10‐8 M. The viability of cells cultured without FBS was a) stimulated by E2 (10‐7 M and 10‐8 M (0.1048 ± 0.0227 and 0.1069 ± 0.0124, respectively)) compared with the control group (0.0566 ± 0.008); b) stimulated by P4 (10‐7 M (0.1088 ± 0.0124)) compared with the control group (0.0566 ± 0.008) and 10‐8 M (0.0924 ± 0.022); and c) stimulated by both concentrations of T (10‐7 M (0.0908 ± 0.0153) and 10‐8 M (0.0924 ± 0.0022)) compared with the control group (0.0566 ± 0.008). Our results demonstrated that FBS stimulated osteoblast viability, and P4 (10‐7 M), and both concentrations of T and E2 stimulated the viability of the cells cultured without FBS, suggesting that these steroid hormones may be important at the onset of osteoblast cells viability in vitro for up to 48 hours.