Effect of Phosphate on the Corrosion of Carbon Steel and on the Composition of Corrosion Products in Two-Stage Continuous Cultures of Desulfovibrio desulfuricans

A field isolate of Desulfovibrio desulfuricans was grown in defined medium in a two-stage continuous culture apparatus with different concentrations of phosphate in the feed medium. The first state (V1) was operated as a conventional chemostat (D = 0.045 h⁻¹) that was limited in energy source (lactate) or phosphate. The second stage (V2) received effluent from V1 but no additional nutrients, and contained a healthy population of transiently starved or resting cells. An increase in the concentration of phosphate in the medium fed to V1 resulted in increased corrosion rates of carbon steel in both V1 and V2. Despite the more rapid corrosion observed in growing cultures relative to that in resting cultures, corrosion products that were isolated under strictly anaerobic conditions from the two culture modes had similar bulk compositions which varied with the phosphate content of the medium. Crystalline mackinawite (Fe₉S₈), vivianite [Fe₃(PO₄)₂ · 8H₂O], and goethite [FeO(OH)] were detected in amounts which varied with the culture conditions. Chemical analyses indicated that the S in the corrosion product was almost exclusively in the form of sulfides, while the P was present both as phosphate and as unidentified components, possibly reduced P species. Some differential localization of S and P was observed in intact corrosion products. Cells from lactate-limited, but not from phosphate-limited, cultures contained intracellular granules that were enriched in P and Fe. The results are discussed in terms of several proposed mechanisms of microbiologically influenced corrosion.     

Interference between dinitrophenyl and azobenzenearsonate determinants on in vitro binding to lymphoid cells. II. Type of binding cells and studies at the level of individual lymphoid cells.

The specific binding of DNP-T₄ on lymphoid cells occurs on the surface of B-cells. This was proved both by the absence of DNP-T₄ binding in cells pretreated with anti-total mouse Ig or anti-mouse IgM sera and by the absence of significant binding on thymocytes. Moreover, splenocytes of nu/nu mice bound similar amounts of DNP-T₄ as splenocytes of CBA/C₃H or BALB/c mice. Removal of adherent cells from normal spleen populations did not decrease the amounts of DNP-T₄ bound onto the non-adherent cell population. Azobenzenearsonate (ARS) conjugates partially inhibited the specific binding of DNP-T₄ to both splenocytes of nu/nu mice and spleen-cell suspensions depleted from adherent cells. The problem of whether the inhibition of specific DNP binding brought about by treatment of the cells with ARS derivatives was expressed by the reduction of the number of binding cells was investigated by two methods. In the first, the number of lytic plaques formed by DNP-T₄ around single lymphoid cells was counted with populations treated or not with ARS derivatives. In the second, anti-TNP producing MOPC-315 cells were used for rosette formation with TNP-conjugated sheep erythrocytes, in the absence or presence of ARS derivatives. Both these methods showed that this inhibition was due to partial reduction of the number of B-cells specifically binding either DNP or TNP determinant, thus indicating that only a certain percentage of the cells bearing the specific hapten receptors are affected by treatment with ARS derivatives.