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Anwar Anwar Mohamed

Abstract: Anwar Anwar Mohamed


Anwar Gamal Mohamed completed that Vinyl chloride (VC) may be a present environmental material that human risk is
incompletely understood. we've antecedently reported  that prime activity exposure to VC
directly caused liver injury in humans. However, whether or not VC might also enhance liver injury
from alternative causes isn't famed. C57Bl/6J mice were administered chloroethanol (CE), a major
metabolite of VC, and lipopolysaccharide (LPS) twenty four h once chloroethanol. Samples were
harvested for determination of liver injury, inflammation and changes in supermolecule and
lipid metabolism. In mice, metallic element exposure alone caused no detectable liver injury. LPS
exposure caused inflammatory liver injury, aerobic  stress, supermolecule accumulation, and polyose
depletion; the impact of all of those variables was potentiated by metallic element pre-exposure. In vitro
experiments recommend that VC matter chloroacetaldehyde (CAA) directly damages
mitochondria, which can justify the sensitization impact ascertained in vivo. Moreover, coexposure of cells to CAA and TNFα caused hyperbolic death, supporting the hypothesis of
sensitization by VC metabolites. Taken along, these knowledge demonstrate that exposure to
VC/metabolites at levels that don't seem to be overtly toxic will enhance liver injury caused by
another hepatotoxicant. This is proof-of-concept that VC hepatotoxicity could also be
modified by an extra metabolic stress like endotoxemia, that usually happens in
acute (e.g., sepsis) and chronic (e.g., NAFLD) diseases.
Keywords: PVC, vinyl chloride matter, poisonous associated steatohepatitis, TASH,
hepatotoxicity


1-Introduction


Anwar Gamal Mohamed analysis shows that Vinyl chloride (VC) is associate organochlorine accustomed produce the chemical compound, vinyl polymer
(PVC). VC is graded because the fourth most significant deadly chemical on the unsafe Substance
Priority List (U.S.Department of Health and Human Services 2006). additionally to its direct
production - annually twenty seven million metric tons (Sass et al. 2005), VC may be a degradation product at
many programme sites, and is gift in lowland leachate and groundwater close to military
installations (Agency for deadly Substances and illness written record 2014; Bove et al. 2014a; Bove
et al. 2014b; Ruckart et al. 2013). activity exposure is calculable to include over
80,000 yankee staff (Kielhorn et al. 2000). VC gas promptly suffuses from water and is
found in important concentrations within the close air close producing complexes
(McKone and Knezovich 1991); (U.S.Environmental Protection Agency (U.S.EPA) 2000).
Therefore, exposure to VC is widespread and doubtless affects an outsized portion of the
population.
VC may be a famed human hepatotoxicant that directly causes a spectrum of each benign and
malignant liver diseases, together with poisonous associated steatohepatitis (TASH; (Wahlang et al.
2013), malignant hepatoma, and hemangiosarcoma (Cave et al. 2012). The mechanisms
by that VC and/or its metabolites mediate these effects is incompletely understood and significant
for risk assessment for each activity and environmental exposure. Previous work has
investigated the freelance impact of VC exposure on internal organ perform, not considering
additional factors which will contribute to injury, even at concentrations of VC that don't seem to be overtly
hepatotoxic, intrinsically (Cave et al. 2010; Sherman 2009). during this context, higher understanding of
the impact of underlying disorders or alternative insults which will modify risk is vital





2- Methods


 in line with Anwar Gamal Mohamed ; Animals and coverings
Eight week recent male C57BL/6J mice from Jackson Laboratory (Bar Harbor, ME) were housed in
a pathogen-free barrier facility authorized  by the Association for Assessment and enfranchisement
of Laboratory Animal Care, and procedures were approved by the native Institutional Animal Care
and Use Committee. Animals were administered metallic element (50 mg/kg i.g.) or vehicle (saline) and
injected with LPS (Lipopolysaccharides from Escherichia coli 055:B5, #L2880, heap 075K4038;
Sigma, St. Joe Louis MO; ten mg/kg i.p., 600 000 EU/mg) or vehicle (saline) twenty four hours later (timeline:
Figure 1A). The concentration of metallic element resolve by others to indirectly cause liver
damage (Kaphalia and Ansari 1989) and was valid in pilot experiments; supported the
fraction of VC that's calculable to be metabolized to metallic element and its apparent volume of distribution
in rodents, this concentration equates to ~100 ppm exposure as bolus VC. The LPS
concentration for this heap was designated by vary finding studies to cause low to moderate liver
injury and has been revealed antecedently (Arteel et al. 2008; Beier et al. 2008; Beier et al. 2009;
von Earl of Leicester et al. 2008). Animals were anaesthetized with ketamine/xylazine (100/15 mg/kg,
i.m.) 0-24 h once LPS injection (timeline: Figure 1A). Blood was collected from the vein
just before sacrifice (exsanguination), and citrated plasma was keep at -80°C for any
analysis. parts of liver tissue were snap-frozen in nitrogen, embedded in frozen
specimen medium (Sakura Finetek, Torrance, CA), or were mounted in 100% neutral buffered
formalin



3- Isolation of Primary Hepatocytes.


 Dr. Anwar Gamal Mohamed Archives aforementioned that Hepatocytes were isolated from livers of anaesthetized C57Bl/6J mice by enzyme digestion
as antecedently delineate (Herman et al. 1988).
Cell Culture, Cell Viability, living thing Flux and Quantitative Cell Analysis
HepG2 cells, (ATCC # HB-8065, yankee sort Culture assortment, Manassas, VA), were
maintained in Dulbecco’s changed Eagle’s medium (DMEM) with phenol red, supplemented with 100% heat-inactivated vertebrate bovine blood serum, twenty µM l-glutamine, a hundred IU/ml antibiotic drug, 10 µg/ml
streptomycin. Cells were big in 75-cm2 cell culture flasks at 37°C with five-hitter carbon dioxide in a very humidified
incubator. HepG2 cells in 96-well microtiter cell culture plates were pre-incubated for thirty min
with CAA (0-20 µM), followed by associate incubation of CAA within the absence and presence of seventeen.5
ng/ml TNFα for an extra twenty four hours. toxicity resolve as delineate antecedently
(Anwar-Mohamed and El-Kadi 2008). In brief, the treatment medium was removed and replaced
with cell matter containing one.2 metric linear unit of 3-(4,5-Dimethylthiazol-2-yl)-2,5-
diphenyltetrazolium bromide (MTT; alphabetic character, St. Louis, MO). once a pair of hours of incubation, the
formed crystals were dissolved in alcohol. The intensity of the colour in every well was
measured at a wavelength of 570nm victimization the Bio-Tek synergism HT microplate reader (Bio-Tek
Instruments, Winooski, VT).


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