Maternal exposure to air pollution and umbilical asprosin concentration, a novel insulin-resistant marker.

Air pollution exposure during pregnancy has been associated with abnormal glucose hemostasis in the fetus, which may result in the programming of type 2 diabetes mellitus (T2DM) development in future life. Therefore, we investigated the association of maternal exposure to particulate matters (PMs) and traffic indicators with umbilical asprosin concentration, a novel insulin-resistant inducing adipokine, in newborns. Accordingly, 759 mother-newborn pairs from Sabzevar, Iran (2018-2019) participated in our study. Maternal exposure to PM1, PM2.5 and PM10 concentrations was estimated using spatial-temporal models developed for the study area. The associations of exposure to traffic indicators (total street length in 100, 300 and 500 m buffers around home and proximity of mothers to nearest major roads) and air pollution with umbilical asprosin concentration were estimated using linear regression models, adjusted for potential confounders. The median (interquartile range (IQR)) of umbilical asprosin concentration was 30.4 (19.1) ng/mL. In fully adjusted models, each one IQR increase in PM10 and PM2.5 were associated with 26.43 ng/mL (95% CI: 10.97, 41.88) and 31.76 ng/mL (95% CI: 15.66, 47.86) increase in umbilical asprosin concentration, respectively. A similarity result was observed for total street length in 100 m buffer. An increase in proximity to major roads was associated with a decrease of -21.48 ng/mL (95% CI: 33.29, -9.67) in umbilical asprosin concentration. Our results suggested that maternal exposure to air pollution during pregnancy could increase the umbilical asprosin concentration. These novel findings may improve our understanding of the mechanisms whereby air pollutants impaired glucose hemostasis during the fetal period.

Paradoxical effect of methimazole on liver mitochondria: In vitro and in vivo.

Methimazole is the most frequently prescribed antithyroid agent. On the other hand, several cases of liver injury are attributed to this drug. The mechanism of methimazole-induced liver injury is obscure. Hepatocytes mitochondria seem to be a target for methimazole cytotoxicity. Current investigation aimed to evaluate the effects of methimazole on the hepatocytes mitochondria in different experimental models. In the in vivo model, methimazole (100, 200 and 400mg/kg, i.p) was administered to mice and liver mitochondria were isolated and assessed. In the in vitro experiments, intact isolated liver mitochondria were incubated with increasing methimazole concentrations (10µM-100mM). It was found that methimazole decreased liver mitochondrial ATP and glutathione, increased mitochondrial swelling, lipid peroxidation and reactive oxygen species (ROS), and collapsed mitochondrial membrane potential when administered to mice. Paradoxically, methimazole not only caused no significant injury toward isolated liver mitochondria in vitro but improved mitochondrial function and protected this organelle. The differences between two investigated models in the current study might be associated with drug bioactivation and reactive metabolites formation. These findings suggest mitochondrial dysfunction as a mechanism for methimazole-induced liver injury. Moreover, methimazole seems to be a novel mitochondrial protecting agent in vitro.

Increased risk of horse sensitization in southwestern Iranian horse riders.

OBJECTIVES: The aim of this study has been to investigate the frequency of sensitization to horse allergens and clinical symptoms in horse riders. MATERIAL AND METHODS: A total of 42 horse riders and 50 healthy individuals were examined by means of skin prick tests for a panel of horse and common animal allergens, and pulmonary function tests were done by spirometry. RESULTS: The rate of sensitization to horse allergens was 31% as proven by the skin prick test in horse riders whereas horse sensitization was not seen in the control group. Occupational allergy symptoms were reported by 19 horse riders. Two horse riders with no history of clinical symptoms showed positive skin reactions to horse allergens. CONCLUSIONS: To decrease the high risk of occupational sensitization among horse riders, workplace conditions should be improved to reduce the load of airborne horse allergens.