Involvement of cd bioaccumulation in spinal deformities occurrence in natural populations of Mediterranean killifish.
ABSTRACT The aim of this study was to investigate the possible influence of environmental exposure to cadmium (Cd) on the spinal deformities occurrence in the Mediterranean killifish, Aphanius fasciatus (Pisces: Cyprinodontidae). For this purpose, some indicators of skeletal bone mineralization, Cd, and calcium (Ca) concentrations in spinal column as well as bioaccumulation of Cd from the water and the sediment have been compared in normal and deformed fish collected from polluted (S1) and nonpolluted (S2) areas in the Gulf of Gabès in Tunisia. When compared to the normal fish, the deformed fish showed signs of spinal column demineralization such as significant decrease in the ash weight/dry weight ratio, percentage of nonorganic components content, and Ca concentration. Cd concentrations in spinal column and liver were significantly higher in deformed fish than in normal fish. A highly significant negative correlation (r = -0.915, p < 0.01) between Cd and Ca concentrations was noted in spinal column of deformed fish. Bioaccumulation factors of Cd in the liver from the water and the sediment in deformed fish were also significantly higher (p < 0.0001) than in normal fish from S1 and S2. These findings suggest that the ability to accumulate large amount of Cd may represent a potential risk to induce spinal deformities in natural populations of Mediterranean killifish.
- [show abstract] [hide abstract]
ABSTRACT: As a simulation of the etiological factors known for Itai-Itai disease, a syndrome characterized by osteomalacia and renal dysfunction in its Japanese victims, female mice were subjected to the individual and combined stresses of dietary cadmium, nutrient-deficient diet, multiparity and ovariectomy; the calcium-depleting effect of each factor was evaluated by determining Ca levels in femur and lumbar vertebrae. At age 68 days, female mice were given nutrient-sufficient (+) or -deficient (-), purified diets containing either 0.25 (environmental), 5, or 50 ppm Cd as CdCl2; the nutritional composition of (-) diet simulated that of food consumed by Japanese victims of Itai-Itai disease. At age 70 days, half of the females began a breeding regimen of six consecutive, 42-day rounds of pregnancy/lactation (PL mice); the remainder were maintained as virgin, non-pregnant controls (NP mice). Limited numbers of PL and NP mice were sacrificed at the end of each reproductive round. PL(+) mice taken at the end of round (R)-6 had successively borne litters in all six rounds, while PL(-) counterparts had nonsuccessively borne only three. At the conclusion of the 252-day reproductive period, remaining females entered the 392-day, post-reproductive phase of the experiment. At age 546 days (mid-R-12), PL females having successfully borne at least three litters were ovariectomized (OV) to mimic human menopause; at the same time, NP females were either ovariectomized or sham-operated (SO). After surgery, all females were maintained to age 714 days (mid-R-16), then sacrificed. During the post-reproductive period, food consumption by females of the same reproductive status was unaffected by elevated levels of Cd or nutrient-deficiencies in diet. However by R-16, Cd at 50 vs. 0.25 ppm had reduced body mass by 11% in both NP and PLOV females, femur and lumbar vertebral calcium content (TCa) by 20 and 25% in the respective groups, and femur and vertebral calcium/dry weight ratios (Ca/DW) by 12 and 11%. Alternative R-16 comparisons indicated that (-) diet also diminished skeletal Ca, but that the additional factors of (prior) multiparity and ovariectomy generated only small and non-significant effects. Comparison of skeletal status between the ends of the reproductive and post-reproductive periods indicated that (1) individual NP groups, regardless of Cd exposure, generally sustained small decreases in TCa and CaDW over time (consistent with aging), but PL groups without exception secured significant gains (consistent with cessation of multiparous activity), (2) skeletal integrity of PL groups was significantly more compromised by the combination of Itai etiological factors at the end of R-6 than R-16, and (3) among those factors, the most demineralizing over lifetime were chronic exposure to Cd followed by ingestion of (-) diet. Despite these findings, skeletal degeneration characteristic of the Itai-Itai syndrome was ultimately not duplicated in this mouse model suggesting that the full-blown disease required primary and profound skeletal demineralization secondarily supported and enhanced by renal dysfunction.Toxicology 05/1997; 119(2):103-21. · 4.02 Impact Factor
- [show abstract] [hide abstract]
ABSTRACT: In order to understand the biological action of cadmium (Cd) in inducing bone pathologies, the effect of Cd on the formation, structure, and properties of hydroxyapatite (HA) in vitro was investigated using three biologically relevant test systems: (1) direct precipitation of HA with no precursor phase; (2) transformation of amorphous calcium phosphate (ACP) to crystalline HA; and (3) growth of HA seed crystals. Cd-containing HA was prepared by transforming ACP to HA in the presence of Cd at a pH of 10; Cd/Ca ratios of 0.05, 0.10, and 0.20 were obtained. Infrared and x-ray diffraction analyses were performed on the Cd-HA samples, and measurements were made of Cd adsorption on HA and of the dissolution characteristics of Cd-containing HA. Cd incorporation in HA introduced little strain in the lattice but resulted in a decreasing C-axis spacing and a corresponding crystal size decrease in the C-axis direction. Cd incorporation had a nominal effect on HA dissolution. Cd had an inhibitory effect on HA formation kinetics in all three test systems. Infrared spectroscopy of Cd-HA showed a complex series of small changes in the spectra as a function of Cd concentration resulting from some distortion in the crystal perfection and symmetry. The interference of Cd with mineralization can be partially explained by its inhibitory effect on HA nucleation and growth in addition to any cellular involvement. Furthermore, Cd probably has little effect on bone mineral dissolution. Our results explain the Cd incorporation reported in bone.Calcified Tissue International 05/1995; 56(4):316-22. · 2.50 Impact Factor
- [show abstract] [hide abstract]
ABSTRACT: It has been determined that zinc supplementation (240 microg Zn/ml) during (for 12 weeks) or after (for 2 weeks) cadmium exposure (50 microg Cd/ml for 12 weeks) can prevent the accumulation and toxic action of Cd in the tibia of rats. The exposure to Cd led to disturbances in bone metabolism reflected by changes in the chemical composition of bone and decreased bone mineral density (osteomalacian changes). The Zn supply in conditions of Cd intoxication completely prevented the Cd-induced increase in percentage of water content and decrease in tibia ash weight, ash weight/dry weight, non-org. comp./org. comp., Zn content and concentration. Moreover, Zn partly protected from the decrease in Ca concentration and content, percentage of non-organic components content, Ca/wet weight, Ca/ash weight and Ca/dry weight. Zn administered after Cd exposure partly, but not completely, protected from Cd-induced decrease in percentage of non-organic components content, Ca/wet weight as well as Ca content and concentration. This protective effect on bone was most evident when Zn was administered during Cd exposure. But Zn, independently of the manner of its administration, did not prevent Cd accumulation in the tibia. Our results suggest that Zn supply in conditions of simultaneous exposure can prevent Cd-induced bone loss to some extent, and used after Cd treatment can give therapeutic benefits.Food and Chemical Toxicology 08/2001; 39(7):729-37. · 3.01 Impact Factor