Effect of Selenium and Vitamin E on the Regeneration of Rat Liver

Maros, T; Fodor, George P.; Kovacs, V.; Katonai, B

doi:10.1093/jn/90.3.219

Cited by 6 publications

(6 citation statements)

References 4 publications

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“…Although the protective effect of 0, (Glynn & Himsworth, 1948) could be due to a competitive reaction between it and an endogenous microsomal process (Slater, 1966), the recent work of Rapin, Got, Le Gall & Goulon (1967) suggests that 0, might affect the regeneration of liver by reducing anoxia after CC1,. Some of the effect of vitamin E on survival may be due to similar causes and this is supported by the work of Butturini et al (1955), Petzold & Weber (1963) and Maros, Fodor, Kovacs & Katonai (1966). Our results suggest also that intraperitoneal injections of antioxidants and vitamin E may function, in part at least, by mechanisms different from those of oral doses, perhaps by stimulating the adrenals.…”

Section: Carbon Tetrachloride Toxicity the Biological Antioxidant Thsupporting

confidence: 86%

Vitamin E and hepatotoxic agents

Cawthorne¹,

Bunyan²,

Sennitt³

et al. 1970

Br J Nutr

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I. The acute toxicity of orally administered CCl, and its subacute toxicity (liver necrosis and hepatic fat accumulation) were studied in young adult male and female rats. CCl, was more toxic in males than in females. The protective effects of vitamin E (D-a-tocopheryl acetate) and three synthetic antioxidants, DPPD (N,N'-diphenyl-p-phenylenediamine), ethoxyquin (6-ethoxy-1,~-dihydro-z,~,4-trimethylquinoline) and BHT (butylated hydroxytoluene) were studied.2. Three daily oral doses (450 mg/kg) of vitamin E given before CCl, increased survival in male rats but not consistently in females. Single oral doses (450 mg/kg) given previously at times between 24 and 72 h were also protective in males, but slightly decreased survival in females. Single intraperitoneal doses (500 mg/kg) given to female rats 1-48 h before CCl, had no effect on survival. None of these treatments with vitamin E significantly decreased CC1,-induced hepatic triglyceride accumulation. A large oral dose (2000 mg/kg) 6 h before CCl, not only significantly increased hepatic fat accumulation but also increased mortality.3. Three daily doses (600 mg/kg) of DPPD or a single oral dose given 72 h before CCl, increased survival in male and female rats. When single doses of DPPD were given 6-48 h before CCl, they had no effect on survival. In contrast, DPPD usually significantly decreased the CC1,-induced hepatic triglyceride rise when given orally 6-72 h before CCl,. Single intraperitoneal doses (1oo-15oo mg/kg) of DPPD, given 1-48 h before CCl,, decreased the hepatic triglyceride rise. Multiple doses of DPPD decreased CC1,-induced liver necrosis, but single doses were generally less effective. 4.Three daily oral doses (300-500 mg/kg) of ethoxyquin given before CCl, were highly effective in preventing mortality, liver necrosis and the rise in hepatic triglycerides. Single oral doses (500 mg/kg) given 72 or 48 h before CCl, produced the same effect, but these single doses 24 or 6 h before CCl, were without effect. The effective treatments usually increased liver weight markedly. Intraperitoneal treatment with ethoxyquin also substantially reduced the toxicity of CC14. Ethoxyquin was the most effective of all four treatments studied, and livers from animals given this substance were often nearly normal in histological appearance.5. The activity of oral doses (400-600 mg/kg) of BHT, given 48 h or more before CCl, was, in general, similar to that of ethoxyquin, but less marked. This substance also caused a large increase in liver weight after 48 h. Oral doses given 6-24 h before CC1, increased the CC1,-induced triglyceride rise still further. Intraperitoneal doses of BHT were ineffective against acute toxicity, liver necrosis or the triglyceride rise.6. Concentrations of a-tocopherol and the three synthetic antioxidants were measured in liver in many of the experiments. Very high hepatic concentrations of a-tocopherol could be obtained without affecting either the acute or subacute toxicity of CCl,. Ethoxyquin and BHT were rapidly eliminated from the liver a...

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Section: Carbon Tetrachloride Toxicity the Biological Antioxidant Thsupporting

confidence: 86%

Vitamin E and hepatotoxic agents

Cawthorne¹,

Bunyan²,

Sennitt³

et al. 1970

Br J Nutr

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“…Alongside hypolipidemic properties of CyC, hypoglycemic effects seen in rats fed a HFD are also supported by previous evidence in vitro and in vivo. In particular, it has been shown that chlorogenic acid (a crucial component of CyC extract used throughout the study) produces inhibition of glucose intestinal absorption, an effect accompanied by marked inhibition of glucose-6-phosphate-translocase [46][47][48], a key enzyme in de novo glucose biosynthesis. This is confirmed by studies revealing that caffeoylquinic acids inhibit glucosidases, thereby explaining the reduction of serum glucose levels found in rats fed a HFD and receiving CyC supplementation [46,47].…”

Section: Discussionmentioning

confidence: 99%

“…This seems to be related to the high concentration of cynaropicrin in CyC extract. Indeed, evidence exists that cynarin and caffeoylquinic acids lead to liver protection in models of liver injury produced by hepatotoxic agents such as carbon tetrachloride, an effect accompanied by reduced oxidative stress and inflammation, as indicated by lower concentrations of liver malondialdehyde and serum transaminases in rats treated with Cynara derivatives [48][49][50]. Moreover, Cynara extract leads to regeneration on injured liver cells, an effect confirmed when using luteolin and other polyphenols [48].…”

Section: Discussionmentioning

confidence: 99%

The Protective Effect of Cynara Cardunculus Extract in Diet-Induced NAFLD: Involvement of OCTN1 and OCTN2 Transporter Subfamily

et al. 2020

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Hyperlipidemia and insulin-resistance are often associated with Non-Alcoholic Fatty Liver Disease (NAFLD) thereby representing a true issue worldwide due to increased risk of developing cardiovascular and systemic disorders. Although clear evidence suggests that circulating fatty acids contribute to pathophysiological mechanisms underlying NAFLD and hyperlipidemia, further studies are required to better identify potential beneficial approaches for counteracting such a disease. Recently, several artichoke extracts have been used for both reducing hyperlipidemia, insulin-resistance and NAFLD, though the mechanism is unclear. Here we used a wild type of Cynara Cardunculus extract (CyC), rich in sesquiterpens and antioxidant active ingredients, in rats fed a High Fat Diet (HFD) compared to a Normal Fat Diet (NFD). In particular, in rats fed HFD for four consecutive weeks, we found a significant increase of serum cholesterol, triglyceride and serum glucose. This effect was accompanied by increased body weight and by histopathological features of liver steatosis. The alterations of metabolic parameters found in HFDs were antagonised dose-dependently by daily oral supplementation of rats with CyC 10 and 20 mg/kg over four weeks, an effect associated to significant improvement of liver steatosis. The effect of CyC (20 mg/kg) was also associated to enhanced expression of both OCTN1 and OCTN2 carnitine-linked transporters. Thus, present data suggest a contribution of carnitine system in the protective effect of CyC in diet-induced hyperlipidemia, insulin-resistance and NAFLD.

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“…At least two of the earliest studies on the artichoke had tried to demonstrate its usefulness in arsenic-poisoned individuals [68]. Artichoke leaf extracts were tested in vivo by Maros [69] to verify their regeneration effects on liver cells. In one experiment, an aqueous artichoke leaf extract, administered orally in partially hepatectomized rats in 0.5 ml/day doses for 21 days, significantly increased liver tissue regeneration as measured from the residual liver weight, mitotic index and liver cell rate.…”

Section: Liver-protecting Actionmentioning

confidence: 99%

Health-promoting properties of artichoke in preventing cardiovascular disease by its lipidic and glycemic-reducing action

Rondanelli

Monteferrario

Perna

et al. 2015

Monaldi Arch Chest Dis

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The artichoke, Cynara scolymus, is one of the most ancient plants grown in the world, and its extracts, obtained from different parts of the plant (leaves, fruits and roots), have been used as medicaments from time immemorial. The pharmacological and therapeutic effects of the artichoke on the liver had already been well known in the 17th century. Modern studies started in the last century confirmed the stimulating properties of artichoke extracts on the liver and gallbladder. The ensuing wave of research was initially focused on the patent liver-stimulating, diuretic and choleretic effects exerted by artichoke preparations on both animals and man, then discovering such other therapeutic properties as the hypolipemizing activity, antioxidant activity and hypoglycemizing activity. This review enumerates the most significant studies that have highlighted these therapeutic properties. Complementary medicine information needs to be incorporated into clinical practice and patient and professional education, in addition to adequate education about proper nutrition. Awareness of the widespread use of complementary and alternative medicine by people with metabolic disorders is crucial for healthcare professionals in order to prevent cardiovascular disease.

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Effect of Selenium and Vitamin E on the Regeneration of Rat Liver

Cited by 6 publications

References 4 publications

Vitamin E and hepatotoxic agents

Vitamin E and hepatotoxic agents

The Protective Effect of Cynara Cardunculus Extract in Diet-Induced NAFLD: Involvement of OCTN1 and OCTN2 Transporter Subfamily

Health-promoting properties of artichoke in preventing cardiovascular disease by its lipidic and glycemic-reducing action

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