Since there are a plethora of studies on cadmium toxicity and poisoning in laboratory animals and humans, we have limited this review to studies that are relevant to human health issues by focusing on carcinogenicity, genotoxicity, circulatory disease, nephrotoxicity and life expectancy. Cadmium exposure has been established to induce cancer in various tissues of laboratory animals. Contrary to early findings of the lack of genotoxicity by cadmium, recent findings of mammalian cell culture studies have revealed genotoxic effects. Furthermore, cadmium exposure at relatively low doses induces circulatory diseases in laboratory animals. Despite such results of various cadmium toxicities in animal studies, data from human studies are lacking and insufficient to support the cause-effect relationship. Although cadmium is currently considered to be a human carcinogen by the International Agency for Research and Cancer, it is inappropriate to conclude that sufficient evidence on the carcinogenicity of cadmium in humans exists. It is also thought that epidemiological studies so far reported do not support the occurrence of cadmium-induced circulatory disease in humans. Since there are inconsistent reports on the relationship of cadmium exposure with the life expectancy of people living in cadmium-polluted areas, further studies are needed for clarification. It is also necessary to examine apparent discrepancies in result between humans and experimental animals. It has been established that long-term exposure to cadmium causes renal dysfunction in both humans and experimental animals, and whether there are any differences in the inducibility of metallothionein in the kidney warrants further study.
We investigated the inhibitory effect of eggplant (Solanum melongena var. marunasu) extract on human fibrosarcoma HT-1080 cell invasion of reconstituted basement membrane [Matrigel (MG)]. We found that the effective component of the plant extract was delphinidin, a flavonoid pigment contained in the peel. The extract and delphinidin did not affect tumor cell adhesion to MG or haptotactic migration to MG. HT-1080 secretes matrix metalloproteinase(MMP)-2 and MMP-9, which degrade extracellular matrix as part of the invasive process. Delphinidin slightly inhibited the activity of MMPs, which may have been responsible, in part, for the inhibition of tumor cell invasiveness.
The hemolytic effects of 27 organotin compounds, which are environmental pollutants, were studied with rabbit erythrocytes. Various EC50 values caused by differences in their chemical structures were observed. The hemolytic activities of tri‐n‐butyltins and triphenyltins were higher than that of sodium‐n‐dodecyl sulfate, and the hemolysis by tri‐n‐butyltin chloride proceeded rapidly. Tri‐n‐butyltin chloride showed the highest hemolytic activity (EC50 = 7.48 μM). Methyltin compounds were less active (EC50>364 μM) than any other organotin compound tested. No significant difference in hemolytic activity based on divergences of the anionic functional group which was attached to each triorganotin compound was observed. A structure–activity relationship study was carried out in order to predict EC50 values of a series of tested organotin compounds, using various descriptors which represent their physicochemical properties or molecular structures. In the multiparametric regression analysis, the best regression equation (r= 0.854) for estimation of their hemolytic effects was obtained by adopting the descriptors Index Value (IV), Mean Information Index (I Dw) and Molecular Connectivity Index (0χp).
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