Role of Kupffer cells in rat liver injury induced by diethyldithiocarbamate

Ishiyama, H.; Oginö, Kazuhíde; Hobara, Tatsuya

doi:10.1016/0926-6917(95)90005-5

Cited by 23 publications

(16 citation statements)

References 24 publications

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“…Such effects are consistent with the antiinflammatory and antineoplastic effects of hypercorticism because a heightened inflammatory response amplifies the toxicity of carcinogens such as carbon tetrachloride (188)(189)(190)(191). Although moderate dietary restriction is recommended for increasing life span and standardizing background tumor incidence between studies (192), excessive dietary restriction, whether a result of reduced food allocation or anorectic effects of the test chemical, should be avoided in cancer bioassays, as such conditions would render the bioassay insensitive for the detection of chemically induced tumors and reduce life expectancy because of the pathologic conditions listed on the right-hand side of Figure 3.…”

Section: Glucocorticoid-mediated Effects Of Caloric Restrictionsupporting

confidence: 61%

Caloric restriction as a mechanism mediating resistance to environmental disease.

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Hart

Leakey

1998

Environ Health Perspect

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It has been observed that susceptibility to many degenerative diseases increases concurrently with industrialization and rising living standards. Although epidemiologic studies suggest that specific environmental and dietary factors may be important, caloric intake alone (as reflected in body size) may account for much of the differential risk observed among diverse human populations. It has been suggested from animal studies that caloric intake may be the primary effector for many hormonal, metabolic, physiologic, and behavioral responses that coordinate reproductive strategy to apparent availability of food. When caloric intake is excessive, particularly at critical developmental stages, physiologic priorities are set for body growth and fecundity rather than for endurance and longevity. The converse occurs during periods of famine, thus increasing the probability that sufficient individuals survive to restore the population when conditions improve. Calorically restricted rodents have significantly longer reproductive and total life spans than their ad libitum-fed controls and exhibit a spectrum of biochemical and physiologic alterations that characterize their adaptation to reduced caloric intake. These include reduced stature, hypercorticism in the absence of elevated adrenocorticotropic hormone levels, increased metabolic efficiency, decreased mitogenic response coupled with increased rates of apoptosis, reduced inflammatory response, induction of stress proteins and DNA repair enzymes, altered drug-metabolizing enzyme expression, and modified cell-mediated immune function. The overall profile of these changes is one of improved defense against environmental stress. This has been suggested as the mechanistic basis for the protective effects of low body weight on radiationand chemically induced cancers in experimental animals. It may also explain the significantly higher thresholds of acute toxicity observed when calorically restricted rodents are exposed to certain test compounds.

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Section: Glucocorticoid-mediated Effects Of Caloric Restrictionsupporting

confidence: 61%

Caloric restriction as a mechanism mediating resistance to environmental disease.

Frame

Hart

Leakey

1998

Environ Health Perspect

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“…36) Activated Kupffer cells are capable of releasing a number of proinflammatory mediators that can activate other cells in the liver (endothelial cells, stellate cells, and hepatocytes), inducing the expression of chemokines, which attract and activate circulating inflammatory cells. 37) One of these proinflammatory mediators is TNF-.…”

Section: Discussionmentioning

confidence: 99%

Biochanin A Protects against Acute Carbon Tetrachloride-Induced Hepatotoxicity in Rats

Breikaa

Algandaby

El‐Demerdash

et al. 2013

Bioscience, Biotechnology, and Biochemistry

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“…Macrophages accumulating in the liver of animals treated with various hepatotoxicants have been reported to release excessive quantities of ROS and RNS (34, 58, 62, 67, 70, 74–76). Moreover, stimulation of macrophages to produce additional oxidants exacerbates liver injury.…”

Section: The Energy Of the Dark Sidementioning

confidence: 99%

Macrophages and Inflammatory Mediators in Chemical Toxicity: A Battle of Forces

Laskin

2009

Chem. Res. Toxicol.

244

231

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Macrophages function as control switches of the immune system, providing a balance between pro- and anti-inflammatory responses. To accomplish this, they develop into different subsets: classically (M1) or alternatively (M2) activated macrophages. Whereas M1 macrophages display a cytotoxic, proinflammatory phenotype, much like the soldiers of The Dark Side of The Force in the Star Wars movies; M2 macrophages, like Jedi fighters, suppress immune and inflammatory responses and participate in wound repair and angiogenesis. Critical to the actions of these divergent or polarized macrophage subpopulations is the regulated release of inflammatory mediators. When properly controlled, M1 macrophages effectively destroy invading pathogens, tumor cells and foreign materials. However, when M1 activation becomes excessive or uncontrolled, these cells can succumb to The Dark Side, releasing copious amounts of cytotoxic mediators that contribute to disease pathogenesis. The activity of M1 macrophages is countered by The Force of alternatively activated M2 macrophages which release anti-inflammatory cytokines, growth factors and mediators involved in extracellular matrix turnover and tissue repair. It is the balance in the production of mediators by these two cell types that ultimately determines the outcome of the tissue response to chemical toxicants.

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Role of Kupffer cells in rat liver injury induced by diethyldithiocarbamate

Cited by 23 publications

References 24 publications

Caloric restriction as a mechanism mediating resistance to environmental disease.

Caloric restriction as a mechanism mediating resistance to environmental disease.

Biochanin A Protects against Acute Carbon Tetrachloride-Induced Hepatotoxicity in Rats

Macrophages and Inflammatory Mediators in Chemical Toxicity: A Battle of Forces

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