Soil organic matter (SOM) as represented in mathematical simulation models involves several hypothetical pools of differing resistance to decay. These conceptual pools satisfy requirements of modeling, but usually have little in common with existing information on physical and chemical properties of SOM. Using our data on turnover times for soil C in fractions of natural aggregates and primary particles, we attempted to relate age of C in physical fractions with that in widely accepted theoretical pools. Soil from a field experiment with 14C‐labeled soybean residues was sampled periodically and separated into physical fractions. The amounts of 14C associated with these fractions at different times provided data for calculation of decay rates and turnover times. The most labile fraction of SOM was plant fragments with turnover time ranging from 1 to 3 yr, which was inversely related to fragment size. Soil aggregates were found to be enriched in C compared with whole soil. This was most pronounced for coarser aggregates whose construction apparently involved the relatively labile plant fragments in some progressive state of decay. The macroaggregates with partially processed C showing turnover from 1 to 3 yr contrasted with microaggregates that included more highly humified C having a longer residence time of ≈7 yr. Various soil fractions differing in residence time of associated C were assembled into several groups that demonstrated consistency with conceptual pools of two widely accepted simulation models. Data from 13C natural abundance studies of soil and of primary fractions were in harmony with models requiring at least two pools of stable SOM.

Summary Decreased membrane rigidity is one of the characteristics of malignant cells, resulting in part from the desaturation of stearic acid into oleic acid. In this study we investigated the influence of stearic acid on tumour cell inhibition in vitro and tumour development in vivo. Stearic acid inhibited the colony-forming ability of 4 out of 5 rat and two human tumour continuous cell lines in vitro. In contrast, the colony-forming ability of rat fibroblasts was not inhibited and that of human foetal lung fibroblasts was inhibited at a higher dose than that required to inhibit human tumour cell lines. Using a model of rat mammary carcinoma induced by nitroso-methyl urea (NMU) the subcutaneous injection of stearic acid at weekly intervals prevented tumour development in 5 to 10 rats. Using iodostearic acid twice weekly, 11 of 19 rats were alive and tumour free at week 22 whilst all of 14 animals injected with NMU alone had died of tumour by the 16th week. The ratio of stearic to oleic acids in erythrocyte membranes was significantly reduced in the tumourbearing rats, but was normal in tumour-free animals treated with stearic or iodostearic acid. These preliminary data indicate that stearic acid inhibits tumour development in rats.The regulation of membrane rigidity is essential for homeostasis (Cooper, 1977) and the metabolic rates of many essential cell enzymes depend on it (Sandemann, 1979). In general, decreased membrane rigidity leads to increased cell metabolism and also higher division rates, features characteristic of the malignant cell. Corvin et al. (1977) have also shown that alteration of membrane lipid structure may change the cancer cell phenotype. The evidence for decreased membrane rigidity in malignant cells is derived from direct physical measurements and lipid analysis. Using fluorescent probes and magnetic resonance studies, decreased microviscosity (decreased membrane rigidity) was found in plasma membranes, as well as in isolated lipid vesicles from leukaemic cells (Petitou et al., 1978;Mountford et al., 1986). Fatty acid analysis of lipids extracted from transformed cells, cell lines, leukaemic cells and solid tumour tissue showed a consistent increase in the oleic acid content relative to stearic acid Wood et al., 1985).The normal metabolic flow results in conversion of the saturated stearic acid to the monounsaturated oleic acid by the enzyme complex delta 9 desaturase. The ratio of stearic to oleic acid, the so-called saturation index (SI), reflects the activity of this enzyme . A significant decrease in the SI of red blood cell membranes was noted in a range of human and animal malignancies (Habib et al., 1987b), and it was suggested that this index could be used as a tumour marker. It has also been reported that there is a decrease in the SI of red blood cell membranes in patients suffering from the Acquired Immune Deficiency Syndrome .We have noted previously that interferon inhibits the desaturation of stearic acid in vitro (Apostolov & Barker, 1981) and that interferon treatment...

Arsenic (As) is toxic for humans, animals, and plants, whereas selenium (Se) is considered as an essential trace element and can cause toxicity during episodic elevated exposure.Interaction between As and Se is a critical factor for a detailed systematic understanding of the transportation, environmental fate, and associated toxicological effects of these metalloids in biological systems. Arsenic and Se induce cytotoxicity and genotoxicity through the generation of reactive oxidation species (ROS). Compared to arsenite (As III ), the methylated arsenicals, including methylarsonous acid (MAs III ) and dimethylarsinous acids (DMAs III ) exhibit more cytotoxic and genotoxic potentials to inhibit more potent enzymes and activate AP˗1 protein, which is a critical marker for genetic stability.Methylated As III and associated metabolites are well-known potential carcinogens that induce toxicity by blocking Se metabolism pathway. Low concentrations of Se compounds under reducing conditions inhibit the DNA repairing process and constraint the binding of zinc finger protein to DNA and ultimately cause the release of zinc from the motif of the zinc finger. Imbalance of Se compounds can lead to the generation of ROS, which can inhibit or decrease genomic stability. Arsenic and Se nexus also affect cellular signaling through activation of the transcription factors such as NFҡB and AP-1. In a nutshell, this review highlights As and Se sources in the environment, their uptake in soil-plant system, interactions between these metals and associated toxicity in major biological compartments, which may assist in addressing the hazardous impacts associated with As and Se contamination. Last but not the lease, this review also summarizes the available remedial measures and future research directions to cope with this critical issue.