We investigated the potential toxicity of gum ghatti, which is added to food for emulsifying, thickening, and stabilizing, after 4 weeks of repeated oral administration at a dose of 8000 mg/kg/day to male and female SD rats. Although food consumption was significantly reduced in males in the gum ghatti group compared with those in the distilled water group from Day 18 onwards, the change was minor, there was no pathological evidence of digestive tract abnormalities, and there were no significant changes in body weight; therefore, the change in food consumption was judged to be of no toxicological significance. Hematology and blood biochemistry revealed statistically significant differences in some parameters between the gum ghatti group and the distilled water group. These changes were all within the normal range of physiological variation and therefore were not considered to represent the effects of gum ghatti. In addition, general signs, body weight, and pathology showed no changes in either sex attributable to gum ghatti. Thus, all changes observed were of no toxicological significance and within the normal range of physiological variation, suggesting gum ghatti has no toxic effects in rats.

The pathological effects of copper deficiency (COD) are well known. However, the pathogenesis of cardiomyopathy resulting from COD remains unclear. In this study, aimed to elucidate the pathogenesis of COD-induced cardiomyopathy by examining the morphology of the cardiovascular system in copper-deficient rats using histopathology, immunohistochemistry, and scanning and transmission electron microscopy. Changes detected in the myocardium and interstitium were consistent with those reported for COD. Morphological changes included mesh-like changes in the capillary endothelial cells that appear to be a novel finding in COD-induced cardiomyopathy. These changes are hypothesized to result from abnormal vascular remodeling following damage to the basement membrane and due to the mechanical effects of myocardial contractions. Although cardiomyopathy may be associated with microcirculatory disorders arising from these lesions, further investigations are necessary to demonstrate a causal relationship between the pathogenesis of cardiomyopathy and the contribution of these lesions to disease progression.