In vitro and in vivo models of acute alcohol exposure

Table 1 The characteristics of in vitro and in vivo models of AAA

AAA model	Advantages	Disadvantages	Area of research
In vitro	Low cost Technically easy to perform Large number of experimental groups Pure cell populations Single cell type or multi-cell type co-culture Strictly controlled settings yielding reproducible results	Limited alcohol metabolism Limited complexity at cellular and tissue levels Limited areas of research, not suitable for behavioral and social studies.	Behavioral and biomedical
In vivo	Availability of physiological routs of alcohol administration Complex interactions of all bodily organs and systems, including complex metabolism Controlled settings, caloric and composition controls Indications to individual and population variability	Ethical concerns High cost Limited information about the effect on one separate cell population.	All areas of research including biomedical, behavioral and social.

Table 2 The effect of acute alcohol abuse on GI system

GI segment	Effect of acute alcohol exposure
Oral cavity	Unknown
Esophagus	Low concentrations of alcohol (up to 5%) cause alterations in ion transports and affect the barrier function
	Concentrations of alcohol of 10% and above cause injury of mucosa
	Co-carcinogenic potency
	Motor dysfunction: decrease in lower esophageal sphincter pressure and amplitude
Stomach	Motor dysfunction: Inhibition of gastric emptying
	Mucosal damage, impaired barrier function, increased epithelial permeability
	Pro-inflammatory reaction: decreased gastric blood flow, vascular damage, polymorphonuclear neutrophils (PMN) dependent- and independent-mucosal damage
	Aggravation of H pylori infection
Intestine	Disruption of barrier function
	Epithelial apoptosis
	Enhanced bioavailability of some alcohol-soluble drugs and impaired absorption of key nutrients
	Increased paracellular intestinal permeability to toxins
Liver	Hepatocytes:
	Amplification of Fas-mediated hepatocyte death
	Generation of oxidative stress
	Hepatic mitochondrial dysfunction
	Increased free iron levels
	Imbalanced fatty acid metabolism
	Inhibition of IFN-α-induced antiviral response towards hepatotropic viruses including hepatitis C virus favors hepatitis C virus replicon expression
	Induced histone H3 acetylation leading to increased gene expression in the liver
	Limited hepatic protein synthesis
	Arrest of liver regeneration early after partial hepatectomy and suppression of hepatic stimulator substance (HSS) activity by induction of liver cell cycle arrest
	Kupffer cells:
	Suppressed LPS-mediated priming for enhanced CC-chemokine release in vitro; up-regulated expression of CC-chemokine mRNA; primed the KC for enhanced RANTES release
	Desensitized HIV-1 gp120-induced CC-chemokine production
	Downregulates HIV-1 glycoprotein 120-induced KC and RANTES production
	Regulates production of reactive oxygen species
	Modulate the tolerance to LPS
	Stellate cells:
	Imbalanced redox potential owed to increased generation of reactive oxygen species upon GSH depletion
Pancreas	Stimulates islet blood flow, amplifies insulin secretion, induces hypoglycemia
	Lower baseline amylase output of acinar pancreatic cells, with the difference being significantly exacerbated by cerulein stimulation
	Interference with release of oxidized proteins in acinar cells
	Predisposes the pancreas to postprandial cholinergic stimulation that triggers cellular events leading to pancreatic inflammation
	Impaired apical exocytosis and redirected exocytosis to less efficient basolateral plasma membrane sites
	Augments elevated-[Ca2+]-induced trypsin activation in pancreatic acinar zymogen granules, leading to premature activation of trypsin and tissue damage