Abstract
The impact of chronic cadmium exposure and slow accumulation on the occurrence and development of diabetes is controversial for human populations. Islets of Langerhans play a prominent role in the etiology of the disease, including by their ability to secrete insulin. Conversion of glucose increase into insulin secretion involves mitochondria. A rat model of pancreatic β-cells was exposed to largely sub-lethal levels of cadmium cations applied for the longest possible time. Cadmium entered cells at concentrations far below those inducing cell death and accumulated by factors reaching several hundred folds the basal level. The mitochondria reorganized in response to the challenge by favoring fission as measured by increased circularity at cadmium levels already ten-fold below the median lethal dose. However, the energy charge and respiratory flux devoted to adenosine triphosphate synthesis were only affected at the onset of cellular death. The present data indicate that mitochondria participate in the adaptation of β-cells to even a moderate cadmium burden without losing functionality, but their impairment in the long run may contribute to cellular dysfunction, when viability and β-cells mass are affected as observed in diabetes.
Highlights
As a widespread contaminant found in the environment, the metal cadmium and its toxicity remain the subject of continuous studies with different approaches
Since the aim of the present study is to probe the sensitivity of the INS-1 cell line upon long-term exposure to sub-lethal concentrations of cadmium, these β-cells were kept for the maximal amount of time in culture in the presence of cadmium before analysis
Considering all the data together, it appears that some characteristics of the INS-1 cell line are sensitive to sub-lethal cadmium concentrations for several generations largely before any sign of significant cellular death is detected
Summary
As a widespread contaminant found in the environment, the metal cadmium and its toxicity remain the subject of continuous studies with different approaches. Low background cadmium contamination in soils, usually below 0.5 ppm, is contributed by dispersion from various sources, such as mining and refining of other metals, waste disposal, and the dispersal of phosphate fertilizers. Cadmium dispersion contaminates crops with cadmium passing through the food chain up to farming animals and human populations. Food is a considerable source of cadmium exposure for humans. Recommendations have been issued and continue to be updated by regulatory bodies to minimize the health effect of cadmium contamination of food and drinking water [2,3]. A major difficulty of the topic is that biological targets of cadmium are numerous [4], and the mechanisms of action of the Cd2+ cation, the only ionic state of biological relevance, can be Toxics 2018, 6, 20; doi:10.3390/toxics6020020 www.mdpi.com/journal/toxics
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