Toxic Cd2 Research Articles

Fertilization and larval development in sea urchins following exposure of gametes and embryos to cadmium.

The gametes and embryos of three sea urchin species were exposed to cadmium chloride at concentrations ranging from 10(-8) M to 10(-3) M. When zygotes were reared in the presence of Cd2+, skeletal differentiation displayed some severe abnormalities or was suppressed, as a function of Cd2+ level. The embryotoxic action of Cd2+ was inversely related to salinity and to Ca2+ concentration. Cadmium-exposed larvae displayed similar abnormalities if Cd2+ was present throughout development or only after hatching, while pre-hatching exposure produced no developmental defects. No aberrations in mitotic figures were observed in cleaving eggs following acute exposure to Cd2+. The pretreatment of sperm or eggs did not affect the ensuing development of embryos, both for acutely toxic Cd2+ levels (up to 10(-2) M), and for prolonged exposures in relatively low Cd2+ levels. The fertilization rate was differently affected depending on whether sperm or eggs were pretreated; i.e., the exposure of eggs to Cd2+ promoted fertilization at relatively high Cd2+ levels. If sperm was exposed to Cd2+, a depression of fertilizing capacity was observed at high Cd2+ levels, while lower Cd2+ levels, displayed an opposite action, resulting in an increase in fertilization rate after prolonged sperm exposure.

Biochemical effects of Cd 2+ -injury in the rat and mouse testis.

Summary. Biochemical changes that occur in the rat or mouse testis after a single subcutaneous injection of a sub-toxic dose of CdCl2 (2·2 μmol/100 g body wt) include decreases in the contents of DNA, RNA and in the activities of certain Zn2+-containing enzymes. The protein content is increased, although the rate of protein synthesis is reduced. Uptake of Cd2+ by the testis is small and does not cause the displacement of Zn2 +. In both species, the concentration of Zn2 + remains constant in the testis for a short time after the parenteral administration of Cd2 +, and then increases progressively. Initially, this increase appears to be due to the decrease in weight of the damaged testis, which is not accompanied by the loss of Zn2+. Later, when the testicular weight becomes constant, Zn2+ continues to accumulate to a level nine to ten times greater than in the normal testis. In the male rat, subcutaneously injected Cd2+ accumulates to high levels and is retained in the liver and kidneys. In both of these organs also, the Zn2+ content increases with the uptake of Cd2+. Bound Cd2+ is present in the soluble components (cell sap) of these tissues as a single fraction, probably metallothionein. This Cd2+-binding protein also accumulates Zn2+ and is responsible for its increased uptake. Competitive antagonism between the toxic Cd2+ cation and the essential Zn2 + ion may occur in the epididymis since, in this organ, the content of the latter cation decreases with the uptake of the former.

Cadmium and zinc binding in mammalian liver and kidneys.

Rats and mice were injected subcutaneousty with cadmium chloride Cd 109 and zinc chloride Zn 65. Both isotopes concentrated primarily in liver and kidneys. Tissue subcellular fractionation showed 70% to 80% 109Cd and 65Zn associated with cytoplasmic soluble fraction. Soluble fraction gel filtration revealed most 109Cd was bound to proteins of 11,000 to 12,000 molecular weight; 65Zn was associated mainly with larger sized molecules. In rats, two weeks following isotope dose, depletion of 65Zn from cytoplasmic macromolecules was demonstrated; 109Cd remained fixed to cadmium-binding proteins (Cd-BP). By ion-exchange chromatography, Cd-BP was resolved into major components. Similar components were separated from human kidney Cd-BP. Presence of Cd-BP was noted in humans and monkey liver tissues. It is suggested that mammalian organism intracellular Cd-BP apparently acts as biochemical mechanism for sequestration of toxic Cd2+ ions.

Relationships Between Corrosion and Fouling of Copper-Nickel Alloys in Sea Water

Voltammetric determination of toxic Cd2+, Pb2+, and Hg2+ metal ions using Cr-BDC/GCE (chromium-benzenedicarboxylates/ Glassy Carbon Electrode) electrochemical sensor has been investigated. Cr-BDC (chromium-benzenedicarboxylate ) metal–organic framework was synthesized by using the facile hydrothermal technique and its efficacy investigated using P-XRD, FTIR, RAMAN, AFM, FE-SEM, and BET, while the electrochemical performance was investigated by CV and EIS technique. The determination capability of Cr-BDC/GCE as an electrochemical sensor has been investigated by DPASV technique. Effective Voltammetric parameters such as pH of buffer solution, pre-accumulation potential, and pre-accumulation time have been optimized to enhance the sensitivity, selectivity, LOD, repeatability, reproducibility, and stability of the sensor. The proposed Cr-BDC/GCE electrochemical sensor exhibits a sensitivity of 16.55, 3.45, and 3.33 µA/M and LOD of 0.186, 0.116, and 0.124 nM for Cd2+, Pb2+ and Hg2+ ions, respectively. Moreover, the sensor exhibited good selectivity, reproducibility, repeatability and stability. The sensor also exhibited good recovery and low RSD values for actual tap water samples. Interaction mechanism of Heavy Metal Ions with the Cr-BDC/GCE evidenced by CV and FTIR confirms the surface adsorption-controlled reaction. These findings suggest that the Cr-BDC/GCE platform is well-suited to serve as a next-generation electrochemical sensor for detecting alcohol, ketone, hydrocarbons, medicines, etc.