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The contamination of feed with mycotoxins is a continuing feed quality and safety issue, leading to significant losses in livestock production and potential human health risks. Consequently, various methods have been developed to reduce the occurrence of mycotoxins in feed; however, feed supplementation with clay minerals or mineral adsorbents is the most prominent approach widely practiced by farmers and the feed industry. Due to a negatively charged and high surface area, pore volume, swelling ability, and high cation exchange capacity, mineral adsorbents including bentonite, zeolite, montmorillonite, and hydrated sodium calcium aluminosilicate can bind or adsorb mycotoxins to their interlayer spaces, external surface, and edges. Several studies have shown these substances to be partly or fully effective in counteracting toxic effects of mycotoxins in farm animals fed contaminated diets and thus are extensively used in livestock production to reduce the risk of mycotoxin exposure. Nevertheless, a considerable number of studies have indicated that these agents may also cause undesirable effects in farm animals. The current work aims to review published reports regarding adverse effects that may arise in farm animals (with a focus on pig and poultry) and potential interaction with veterinary substances and nutrients in feeds, when mineral adsorbents are utilized as a technological feed additive. Furthermore, results of in vitro toxicity studies of both natural and modified mineral adsorbents on different cell lines are reported. Supplementation of mycotoxin-contaminated feed with mineral adsorbents must be carefully considered by farmers and feed industry.

The aging process and its characterization in keratinocytes have not been studied in depth until now. We have assessed the cellular and molecular characteristics of aged epidermal keratinocytes in monolayer cultures and in skin by measuring their morphological, fluorometric and biochemical properties. Light and electron microscopy, as well as flow cytometry, revealed increase in cell size, changes in cell shape, alterations in mitochondrial structure and cytoplasmic content with aging. We showed that the expression of 16 biochemical markers was altered in aged cultured cells and in tissues, including caspases 1 and 3 and beta-galactosidase activities, immunoreactivities of p16, Ki67, 20S proteasome and effectors of the Fas-dependent apoptotic pathway. Aged cells diversity, and individual variability of aging markers, call for a multifunctional assessment of the aging phenomenon, and of its modulation by drugs. As a test case, we have measured the effects of Dead Sea minerals on keratinocyte cultures and human skin, and found that they stimulate proliferation and mitochondrial activity, decrease the expression of some aging markers, and limit apoptotic damage after UVB irradiation.

Cardiovascular mortality is significantly increased among patients with end-stage renal disease. The commonly observed vascular calcification in such patients has been considered as one of the causative factors. In patients undergoing dialysis, the incidence of coronary artery calcification is 2-5 times higher compared to patients with normal renal function and angiographically demonstrated coronary artery disease. Moreover, epidemiological studies have revealed a significant correlation of the extent of coronary artery calcification with the severity of underlying atherosclerotic lesions. Vascular calcification was initially considered as a passive process of hydroxyapatite deposition due to elevated plasma concentrations of calcium and phosphate. Nevertheless, there is a growing body of evidence that vascular calcification is an actively regulated and cell-mediated process. This phenomenon includes phenotypic alterations of vascular smooth muscle cells mainly resulting from an imbalance between promoters (such as increased Ca x P product) and inhibitors (fetuin-A, GLA protein, osteoprotegerin) of mineral deposition. With regard to the therapeutic approach, despite the evident effectiveness of both traditional and innovative remedies in the management of metabolic and electrolytic abnormalities of patients with end-stage renal disease, an individualized intervention based on etiopathogenesis is really required.

Bone morphogenetic proteins (BMPs) are known to promote periodontal tissue regeneration, while noggin inhibits the biological activities of BMP-2, -4, and -7. To investigate the effect of BMPs and noggin gene transfer on cementogenesis, we used cloned murine cementoblasts (OCCM). Cells were transduced using adenoviruses encoding BMP-7 (Ad-BMP-7), noggin devoid of the heparin binding site (Ad-NOGDeltaB2), or a control adenovirus encoding green fluorescent protein (Ad-GFP). Cells were seeded into 3D polymer scaffolds and implanted into SCID mice to determine the in vivo mineral-inducing ability of the cells. Cells transduced with Ad-NOGDeltaB2 at 3 and 6 weeks postimplantation exhibited reduced mineral formation compared with all other groups. Although gene expression of osteocalcin and bone sialoprotein increased after Ad-BMP-7 transduction in vitro, following BMP-7 gene transfer in vivo, transcripts for OCN and BSP were not significantly different from controls, and mineral density was not significantly increased compared with Ad-GFP and NT groups. These results indicate that in mature cementoblast populations, gene transfer of noggin inhibits biomineralization induced by cementoblasts, whereas exogenous BMP has minimal effects on mineralization.

Interactions between vitamin A and vitamin D have been suggested for several decades but have not been established. In particular, vitamin A has been proposed to intensify the severity of the bone mineralization disease, rickets and inhibit the ability of vitamin D to cure this disease. To investigate this hypothesis, weanling Holtzman rats were fed a 1.2% calcium, 0.1% phosphorus diet and 15.5 ng ergocalciferol (vitamin D(2)) every 3 d for 21 d in the presence of increasing amounts of retinyl acetate (0 microg to 8621 microg/d). The increasing amounts of retinyl acetate produced a progressive and significant decrease in total bone ash (P < 0.001) and an increase in epiphyseal plate width (P < 0.001). The same experiment conducted with increasing amounts of vitamin D(2) (0 to 645 ng/d) indicated that the antagonism by retinyl acetate could be demonstrated at all vitamin D(2) dosages. To further investigate this antagonistic relationship, weanling Holtzman rats were fed a 0. 47% calcium, 0.3% phosphorus diet and 15.5 ng vitamin D(2) every 3 d for 33 d in the presence of increasing retinyl acetate (0 to 3448 microg/d). In the absence of retinyl acetate, these rats maintained a normal serum calcium level (2.34 mmol/L). Increasing retinyl acetate, however, eliminated the ability of vitamin D(2) to elevate the level of serum calcium (1.35 mmol/L). These results illustrated in vivo antagonism of vitamin D(2) action on intestine and bone by retinyl acetate.