No abstract

Samples of liver, renal cortex, and medulla were obtained from 55 forensic autopsies (0- to 95-yr-old Japanese). Metallothionein (MT) was determined by the Ag-hem or Cd-hem method. Zinc (Zn), copper (Cu), and cadmium (Cd) were determined by atomic absorption spectrophotometry. The mean levels of MT were 250 micrograms/g in the liver, and 394 micrograms/g (cortex) and 191 micrograms/g (medulla) in the kidney. Age-dependent changes were observed in both the liver and kidney. In the liver, MT level decreased during infancy and increased thereafter with age. Similar age-dependent changes in the levels of Zn and Cu were observed. In the kidney cortex, MT level increased with age, although no correlation was found after middle age. The levels of Cd and Zn also increased with age until middle age; however, they decreased thereafter. These results suggest that age-dependent changes in renal MT levels are associated with accumulation of Cd.

Evidence indicates that the presence of aberrant α1→2fucosylation pathways is responsible for the accumulation of large quantities of Leb and Y antigens in human colorectal carcinoma. Significantly higher activities of α1→2 as well as α1→3 and α1→4fucosyltransferases were found in most of the tissues from carcinoma than in the adjacent normal tissues and in healthy subjects. α1→2Fucosyl‐transferases associated with the synthesis of Leb (Fucal→2Galβ1→3[Fucc1→4]GlcNAcβ) and Y (Fucα1→2Ga1β→4[Fucα1→3]GlcNAcβ) structures from Le→ (GaIβ1→3[Fucal→4]GlcNAcβ) and X (Galβ1→4[Fucα 1→3]GlcNAcβ) ones, respectively, were demonstrated in colorectal carcinomas and in colorectal carcinoma cell lines (COLO201, LS174T and SW1116). The activation of α1→2fucosyltransferase with such new substrate specificities in colorectal carcinoma might result in the preferential synthesis of Leb and Y structures from Le→ and X rather than from H type 1 and H type 2 structures.

No abstract

Hydrogen sulfide (H₂S) is a toxic gaseous substance, and accidental exposure to high concentrations of H₂S has been reported to be lethal to humans. Inhaled and absorbed H₂S is partially dissolved within the circulation and causes toxic effects on lymphocytes. However, the mechanisms involved in H₂S toxicity have not been well documented. In this study, we examined the cellular uptake and injury of sulfide-exposed human T lymphocytes (Jurkat). Cells were exposed to a H₂S donor, sodium hydroxysulfide (NaHS), at pH 6.0, 7.0, or 8.0 for 1 h at 37 °C in a sealed conical tube to avoid the loss of dissolved H₂S gas. Cytotoxicity and cellular sulfide concentrations increased dramatically as the pH of the NaHS solution decreased. Sulfide enhanced the cleavage of caspase-3 and poly (ADP-ribose) polymerase and induced early cellular apoptosis. A pan-caspase inhibitor reduced sulfide-induced apoptosis. These results indicate that sulfide induces pH-dependent and caspase-dependent apoptosis. We also found that blebbing of the plasma membrane occurred in sulfide-exposed cells. Both ROCK-1 and ROCK-2 (Rho kinases) were activated by sulfide, and sulfide-induced cell blebbing was suppressed by a ROCK inhibitor, suggesting that a Rho pathway is involved in sulfide-induced blebbing in lymphocytes.