Oxidative damage and fumonisin B1-induced toxicity in primary rat hepatocytes and rat liver in vivo

Abel, Stefan; Gelderblom, Wentzel C. A.

doi:10.1016/s0300-483x(98)00123-1

Cited by 141 publications

(87 citation statements)

References 31 publications

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“…In contrast, Abel and Gelderblom (1998) showed that FB 1 contaminations at doses of 10, 50 and 100 mg/kg feed for 21 days, respectively, did not adversely affect the body weight gain and the relative liver weight; this effect was only found at doses of 250 and 500 mg/kg feed. Abel and Gelderblom (1998) found a lowered feed intake only at an FB 1 concentration of 250 mg/kg feed, and in the 21-day study the feed intake reached the control level after 14 days. It is thus a new finding of the present study that even an FB 1 dose of 50 mg/kg feed has an adverse effect on the feed intake, and this occurs as early as three days after toxin administration.…”

Section: Body Weight Liver Weight Feed Intakementioning

confidence: 79%

“…In an earlier study Abel and Gelderblom (1998) reported significantly increased thiobarbituric acid reactive substance (TBARS) level as a result of 250 and 500 mg/kg FB 1 exposure in the feed for 21 days, causing damage to cellular and microsomal membranes as well. Perhaps this was the first hint that FB 1 sensitises hepatocytes toward oxidative stress.…”

mentioning

confidence: 99%

“…As a consequence, emerging free radicals induce hepatocellular damage and metabolic abnormalities. Based on the above information, Abel and Gelderblom (1998) classified FB 1 as a hepatotoxic but non-genotoxic compound in rats. Sahu et al (1998) studied whether FB 1 affects nuclear membranes and DNA in the rat liver, and confirmed the induction of nucleolemmal lipid peroxidation as well as DNA strand breaks.…”

mentioning

confidence: 99%

“…As far as the authors are aware, the acute effects of FB 1 have only been tested in vitro (24-48 h; Abel and Gelderblom, 1998). Since those settings are hardly comparable with an in vivo trial, we aimed to test the acute effects of a relatively low but realistic dose of FB 1 (50 mg/kg feed) using an exposure that lasted for only 5 days.…”

mentioning

confidence: 99%

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Acute hepatic effects of low-dose fumonisin B1 in rats

Szabó

Szabó-Fodor

Fébel

et al. 2016

Acta Veterinaria Hungarica

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Adult male Wistar rats were enrolled in a study to test the acute hepatic effects of 50 mg/kg fumonisin B 1 in feed for 5 days. Fumonisin B 1 depressed growth and feed intake, and absolute and relative liver weight showed a significant increase. The proportions of C17:0, C18:3 n3, C22:5 n3 and C22:6 n3 fatty acids decreased in the hepatic phospholipid fraction. All proportional decreases modified the hepatocellular membrane lipids into a more rigid state. The fatty acid profile modifications were partly compensated for by endogenous glutathione (preventing the formation of conjugated dienes and trienes as initial phase lipid peroxidation indicators), while the enzymatic antioxidant defence system (glutathione peroxidase) was unaltered. In contrast, hepatic malondialdehyde, the cytotoxic product of end-phase lipid peroxidation showed a concentration increase even after 5 days of feeding. The results indicate a rather strong and rapid hepatic effect of FB 1 , immediately impairing membrane phospholipids, even before the enzymatic antioxidant defence is activated.Key words: Fumonisin B 1 , rat, hepatocellular membrane, fatty acids, oxidative stress, antioxidants Fumonisins are cancer-inducing metabolites of Fusarium proliferatum and Fusarium verticillioides. They have a long-chain hydrocarbon unit (mimicking to a certain extent cellular sphingosine and sphinganine), which plays a determinant role in their cell-membrane-associated toxicity. From the fumonisin group, fumonisin B 1 (FB 1 ) shows strong toxic effects and has been reported to promote hepatic tumour in rats. Fumonisin B 1 , the most abundant of the numerous fumonisin analogues, was classified by the IARC as a Group 2B carcinogen (possibly carcinogenic in humans; IARC, 2002).

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Section: Body Weight Liver Weight Feed Intakementioning

confidence: 79%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Acute hepatic effects of low-dose fumonisin B1 in rats

Szabó

Szabó-Fodor

Fébel

et al. 2016

Acta Veterinaria Hungarica

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“…For example, several groups have presented data suggesting that fumonisins cause compositional or oxidative damage to cellular lipids, which in turn causes molecular events culminating in oxidative damage to DNA and other critical macromolecules (94)(95)(96)(97)(98)(99). A more detailed discussion of molecular mechanism is beyond the purpose of this review but can be found elsewhere in this issue (87,(100)(101)(102).…”

Section: Fumonisins and Sphingolipids: Mechanistic Considerationsmentioning

confidence: 99%

An overview of rodent toxicities: liver and kidney effects of fumonisins and Fusarium moniliforme.

Voss

Riley

Norred

et al. 2001

Environ Health Perspect

122

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Fumonisins are produced by Fusarium moniliforme F. verticillioides) and other Fusarium that grow on corn worldwide. They cause fatal toxicoses of horses and swine. Their effects in humans are unclear, but epidemiologic evidence suggests that consumption of fumonisin-contaminated corn contributes to human esophageal cancer in southern Africa and China. Much has been learned from rodent studies about fumonisin B1(FB1), the most common homologue. FB1 is poorly absorbed and rapidly eliminated in feces. Minor amounts are retained in liver and kidneys. Unlike other mycotoxins, fumonisins cause the same liver cancer promotion and subchronic (studies (3/4) 90 days) liver and kidney effects as (italic)F. moniliforme. FB 1 induces apoptosis of hepatocytes and of proximal tubule epithelial cells. More advanced lesions in both organs are characterized by simultaneous cell loss (apoptosis and necrosis) and proliferation (mitosis). Microscopic and other findings suggest that an imbalance between cell loss and replacement develops, a condition favorable for carcinogenesis. On the molecular level, fumonisins inhibit ceramide synthase, and disrupt sphingolipid metabolism and, theoretically, sphingolipid-mediated regulatory processes that influence apoptosis and mitosis. Liver sphingolipid effects and toxicity are correlated, and ceramide synthase inhibition occurs in liver and kidney at doses below their respective no-observed-effect levels. FB1 does not cross the placenta and is not teratogenic in vivoin rats, mice, or rabbits, but is embryotoxic at high, maternally toxic doses. These data have contributed to preliminary risk evaluation and to protocol development for carcinogenicity and chronic toxicity studies of FB1 in rats and mice.

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Mycotoxins with a Special Focus on Aflatoxins, Ochratoxins and Fumonisins

Steyn

Gelderblom

Shephard

et al. 2009

General, Applied and Systems Toxicology

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Mycotoxins are important environmental and carcinogenic agents. They are ubiquitous in a broad range of commodities and cause toxic responses when ingested by humans and animals. A review of mycotoxins is presented with special reference to the producing species, analytical methodology, occurrence, biological activity, decontamination, regulations and the risk assessment of aflatoxins, ochratoxins and fumonisins. Some of the most recent studies regarding the mechanisms involved in fumonisin B 1 ‐induced biological effects in different cell culture systems are tabulated. The review is directed at updating the previous review of Steyn and Stander (1999) with a focus on recent findings.

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Oxidative damage and fumonisin B1-induced toxicity in primary rat hepatocytes and rat liver in vivo

Cited by 141 publications

References 31 publications

Acute hepatic effects of low-dose fumonisin B1 in rats

Acute hepatic effects of low-dose fumonisin B1 in rats

An overview of rodent toxicities: liver and kidney effects of fumonisins and Fusarium moniliforme.

Mycotoxins with a Special Focus on Aflatoxins, Ochratoxins and Fumonisins

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