Trace elements status in diabetes mellitus type 2: possible role of the interaction between molybdenum and copper in the progress of typical complications.

It is well established that both, the deficiency and possible overload of mineral micronutrients have adverse health effects. It is also generally accepted that non-essential xenobiotics contribute to oxidative damage, which is considered one of the principal factors in diabetes and its complications. The purpose of this work was to gain an insight on the global role of metal/metalloids in the progress of diabetes mellitus type 2. In such approach, aluminum, vanadium, chromium, manganese, cobalt, nickel, copper, zinc, arsenic, selenium, molybdenum, mercury, cadmium and lead were determined by inductively coupled plasma-mass spectrometry (ICP-MS) in serum and urine of 76 diabetic patients (age 52 ± 8 years, 5-16 years of DM2, 52 subjects with slight-to-moderate complications and 24 with severe complications). A series of anthropometric and clinical parameters usually evaluated in the follow-up of patients were assessed by standard methods. Statistical analysis (unpaired t-test, analysis of correlation and principal component analysis) was then carried out in search of possible relationships existing among metals/metalloids and these parameters. The results obtained suggest that antagonistic interaction between molybdenum and copper might be involved in the progress of diabetes complications.

Molybdenum in human whole blood of adult residents of the Merida State (Venezuela).

The concentration of molybdenum was measured in whole blood samples of 418 (244 males and 174 females) apparently normal donors ranging in age from 18 to 27-years old and living in nine different locations in the Mérida State (Venezuela). The geometric mean concentration of molybdenum of 418 subjects was of 2.66+/-0.66 microgL(-1) (range: 1.20-4.80 microgL(-1)). The levels of molybdenum in whole blood samples found in this work were of 2.57+/-0.52 and 2.54+/-0.51 (range: 1.20-4.80 and 1.40-4.20) microgL(-1) for males and females, respectively. The data of the content molybdenum in whole blood had no statistical correlation with age, sex or height above the sea level of the sampling sites. However, there was a tendency to decrease the levels of the element in those sampling sites located in highlands (> or = 1900 m above the sea level). This variability may be due to the source of molybdenum from the soil to the food chain that has affected its levels in donors from these areas under study. The results of this study are compared with values previously reported for subjects studied in other populations.

[Experimental model for the study of molybdenosis in the primary copper deficiency in rats]. / Modelo experimental para el estudio de la molibdenosis y de la deficiencia primaria de cobre en ratas.

An experimental model in rats was evaluated to differentiate the effects between Copper deficiency and Molybdenosis. Sixty weaning rats (30 male and 30 female) received a diet with 70% complete powder milk (1 ppm Cu) and 30% maize meal (0.8-1.5 ppm Cu). Three experimental groups received the following mineral supplementation: copper deficiency (40 ppm Fe), molybdenosis (40 ppm Fe + 40 ppm Cu + 500 ppm Mo) and control (40 ppm Fe + 40 ppm Cu). The animals were weighed each 14 days. At 70 days of treatment were sacrificed. Blood and liver were sampled for analyzing hematocrit, ceruloplasmin activity and Cu and Mo liver concentration. Copper deficiency group had less serum ceruloplasmin activity. Cu and Mo liver concentration were higher in the animals with molybdenosis. We concluded that when Cu levels are higher than minimum requirement, feeding with high Mo, do not affect ceruloplasmin activity. In addition, high Mo liver concentration allows us to elucidate effects "per se" of molybdenosis.