Role of glutathione in protection against mercury induced poisoning

Mercury is harmless in an insoluble form, such as mercuric sulfide, but it is poisonous in soluble forms such as mercuric chloride or methylmercury. Mercury is a neurotoxin. Outbreaks of mercuric chloride poisonings have made it clear that adults, children, and developing fetuses are at risk from ingestion exposure to mercury. It is very important and interesting to study the reaction of mercuric chloride and Glutathione as biomarker of Glutathione role in detoxification and conjugation in components [Plasma and Cytosolic Fraction]. The effect of mercuric chloride's different concentrations was examined on GSH present in plasma and cytosolic fraction. Decrease in GSH level was dependant on mercuric chloride concentration. The decrease in GSH level of blood components was more prominent with the time of incubation of mercuric chloride. Decrease in the concentration of reduced state Glutathione may be due the interaction of reduced state Glutathione [GSH] and mercuric chloride to form oxidized Glutathione [GSSG] or mercuric-glutathione complex. This change in GSH metabolic status provides information regarding the role of GSH in detoxification of mercuric chloride. The effect of mercury metal on Glutathione in blood components has been discussed in this paper in vitro condition as a model for in Vivo condition

Toxicological response of phormidium fragile to mercury

The effects of different concentrations of mercury on cyanobacterium Phormidium fragile were studied. The results revealed that dry biomass yield, protein content, chlorophyll a and carotenoids decreased with an increased concentration of mercury from 0.01 to 1.5 ppm. Also, malate dehydrogenase [MDH], glutamate dehydrogenase [GIDH] and nitrate reductase activity were affected by an increased metal concentration, whereas glutamic-oxalacetic transaminase [GOT] and glutamic-pyruvic transaminase [GFT] were hardly affected. Mercury uptake increased at the higher levels of the metal. On the other hand, all the amino acid components gradually increased with the rise of the metal level, except isoleucine, histidine and methionine which were suppressed by the smaller doses and completely disappeared by the larger doses of the metal

Inhibition of luminol-dependent chemiluminescence of human granulocytes by low doses of inorganic mercury

HgCl2, added in vitro to human granulocytes in whole blood, caused a marked inhibitory effect on the luminol-dependent chemiluminescence induced by BaS04 crystals in suspension of these cells. The effect was both dose- and time-dependent when BaS04 was used to stimulate the oxidative burst in granulocytes. Incubation with the highest concentration of HgCl2 used [10 mmol/L], however, did not cause disruption of the membranes of granulocytes. The effect of HgCl2 on the granulocytes was irreversible following washing of the HgCl2-treated cells with phosphate buffered saline. HgCl2 did not affect chemiluminescence produced when luminol was excited by oxidative hydrogen peroxide in a cell-free medium. These results suggest that some of the toxicity of HgCl2 may be greater than mediated by an action on the phagocytic immune system