Cholinestarase activity in methylmercury and mercury chloride exposure fish

2013 ◽  
Vol 8 (1) ◽  
pp. 147-148
Author(s):  
Jesus T.B. ◽  
Colombi J.S. ◽  
Ribeiro C.A.O. ◽  
Assis H.C.S. ◽  
Carvalho C.E.V.
Keyword(s):  
Mercury Chloride

scholarly journals Transcriptome Analysis Reveals HgCl2 Induces Apoptotic Cell Death in Human Lung Carcinoma H1299 Cells through Caspase-3-Independent Pathway

2021 ◽  
Vol 22 (4) ◽  
pp. 2006
Author(s):  
Mi Jin Kim ◽  
Jinhong Park ◽  
Jinho Kim ◽  
Ji-Young Kim ◽  
Mi-Jin An ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Transcriptome Analysis ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Expression Patterns ◽  
Nitrogen Compound ◽  
Apoptotic Cell Death ◽  
Mercury Chloride ◽  
Rna Seq

Mercury is one of the detrimental toxicants that can be found in the environment and exists naturally in different forms; inorganic and organic. Human exposure to inorganic mercury, such as mercury chloride, occurs through air pollution, absorption of food or water, and personal care products. This study aimed to investigate the effect of HgCl2 on cell viability, cell cycle, apoptotic pathway, and alters of the transcriptome profiles in human non-small cell lung cancer cells, H1299. Our data show that HgCl2 treatment causes inhibition of cell growth via cell cycle arrest at G0/G1- and S-phase. In addition, HgCl2 induces apoptotic cell death through the caspase-3-independent pathway. Comprehensive transcriptome analysis using RNA-seq indicated that cellular nitrogen compound metabolic process, cellular metabolism, and translation for biological processes-related gene sets were significantly up- and downregulated by HgCl2 treatment. Interestingly, comparative gene expression patterns by RNA-seq indicated that mitochondrial ribosomal proteins were markedly altered by low-dose of HgCl2 treatment. Altogether, these data show that HgCl2 induces apoptotic cell death through the dysfunction of mitochondria.

scholarly journals In Vivo Functional Assay of a Recombinant Aquaporin in Pichia pastoris

2006 ◽  
Vol 72 (2) ◽  
pp. 1507-1514 ◽  
Author(s):  
Mark J. Daniels ◽  
Malcolm R. Wood ◽  
Mark Yeager
Keyword(s):  
Pichia Pastoris ◽  
Linear Relationship ◽  
Osmotic Shock ◽  
Water Channel ◽  
Yeast Cells ◽  
Mercury Chloride ◽  
Functional Assay ◽  
Channel Activity ◽  
Wild Type

ABSTRACT The water channel protein PvTIP3;1 (α-TIP) is a member of the major intrinsic protein (MIP) membrane channel family. We overexpressed this eukaryotic aquaporin in the methylotrophic yeast Pichia pastoris, and immunogold labeling of cellular cryosections showed that the protein accumulated in the plasma membrane, as well as vacuolar and other intracellular membranes. We then developed an in vivo functional assay for water channel activity that measures the change in optical absorbance of spheroplasts following an osmotic shock. Spheroplasts of wild-type P. pastoris displayed a linear relationship between absorbance and osmotic shock level. However, spheroplasts of P. pastoris expressing PvTIP3;1 showed a break in this linear relationship corresponding to hypo-osmotically induced lysis. It is the difference between control and transformed spheroplasts under conditions of hypo-osmotic shock that forms the basis of our aquaporin activity assay. The aquaporin inhibitor mercury chloride blocked water channel activity but had no effect on wild-type yeast. Osmotically shocked yeast cells were affected only slightly by expression of the Escherichia coli glycerol channel GlpF, which belongs to the MIP family but is a weak water channel. The important role that aquaporins play in human physiology has led to a growing interest in their potential as drug targets for treatment of hypertension and congestive heart failure, as well as other fluid overload states. The simplicity of this assay that is specific for water channel activity should enable rapid screening for compounds that modulate water channel activity.

Bioresilience to Mercury Chloride of the Brine Shrimp Artemia Salina after Treatment with Homeopathic Mercurius Corrosivus

Homeopathy ◽  
2021 ◽  
Author(s):  
Andreia Adelaide G. Pinto ◽  
Mirian Y. de Oliveira Nagai ◽  
Ednar Nascimento Coimbra ◽  
Suham Nowrooz Mohammad ◽  
Jefferson Souza Silva ◽  
...  
Keyword(s):  
Sea Water ◽  
Specific Interaction ◽  
Artemia Salina ◽  
Mercury Content ◽  
Mercury Chloride ◽  
Hatching Rate ◽  
Toxic Substances ◽  
Protective Effects ◽  
Cyst Hatching ◽  
The Impact

Abstract Introduction Finding solutions to mitigate the impact of pollution on living systems is a matter of great interest. Homeopathic preparations of toxic substances have been described in the literature as attenuation factors for intoxication. Herein, an experimental study using Artemia salina and mercury chloride was developed as a model to identify aspects related to bioresilience. Aims The aim of the study was to describe the effects of homeopathic Mercurius corrosivus (MC) on Artemia salina cysts hatching and on mercury bioavailability. Methods Artemia salina cysts were exposed to 5.0 µg/mL of mercury chloride during the hatching phase. MC potencies (6cH, 30cH, and 200cH) were prepared in sterile purified water and poured into artificial sea water. Different controls were used (non-challenged cysts and challenged cysts treated with water, succussed water, and Ethilicum 1cH). Four series of nine experiments were performed to evaluate the percentage of cyst hatching. Soluble total mercury (THg) levels and precipitated mercury content were also evaluated. Solvatochromic dyes were used to check for eventual physicochemical markers of MC biological activity. Results Significant delay (p < 0.0001) in cyst hatching was observed only after treatment with MC 30cH, compared with controls. This result was associated with an increase of THg concentration in water (p = 0.0018) and of chlorine/oxygen ratio (p < 0.0001) in suspended micraggregates, suggesting changes in mercury bioavailability. A specific interaction of MC 30cH with the solvatochromic dye ET33 (p = 0.0017) was found. Conclusion Changes in hatching rate and possible changes in Hg bioavailability are postulated as protective effects of MC 30cH on Artemia salina, by improving its natural bioresilience processes.

scholarly journals Histomorphological effect of ascorbic acid on mercury chloride-induced changes on the cerebellum of adult wistar rats

2014 ◽  
Vol 31 (04) ◽  
pp. 219-224 ◽  
Author(s):  
A. Ibegbu ◽  
A. Animoku Abdulrazaq ◽  
Ayuba Micheal ◽  
Brosu Daniel ◽  
A. Adamu Sadeeq ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Cerebellar Cortex ◽  
Wistar Rats ◽  
Oral Route ◽  
Mercury Chloride ◽  
Average Weight ◽  
The Central Nervous System ◽  
Living Organisms ◽  
Induced Changes ◽  
Acid Administration

Abstract Introduction. Mercury is one of the most hazardous environmental contaminants to living organisms and the central nervous system has been shown to be the main target. Objective. The present work was aimed at evaluating the effect of ascorbic acid on mercury chloride-induced changes on the cerebellar cortex of adult Wistar rats. Material and method. Thirty Wistar rats of average weight of 200g and were randomly divided into 6 groups of 5 rats each. The animals in Group 1 (control) were administered with distilled water, Groups 2 and 3 were administered with 52mg/kg and 26.25mg/kg body weight of HgCl respectively while Groups 4 and 5 were administered with 52mg/kg of HgCl and 5mg/kg of ascorbic acid and 26.25gm/kg of HgCl and 5mg/kg of ascorbic acid respectively, while Group 6 was administered with 5mg/kg of ascorbic acid. The administration was through oral route, daily for 3 weeks. Results. The result of the biochemical parameters showed a significant increase (P < 0.05) on the mean SOD and LPO values after the administration of mercury chloride and Ascorbic acid. Histological observation of the cerebellar cortex, showed normal histo-morphology in Groups 1 and 6 while, the cerebellum in Groups 2, 3, 4 and 5 showed some degenerative, necrotic and cellular changes. Conclusion. However, ascorbic acid administration has shown to ameliorate the induced degenerative changes in the cerebellum caused by mercury chloride toxicity in Wistar rats.

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