Ascorbic Acid Protects Guinea Pigs from Acute Aflatoxin Toxicity

Sp, Netke; Mw, Roomi; Tsao, Chao Jung; Niedzwiecki, Aleksandra

doi:10.1006/taap.1996.8091

Cited by 57 publications

(35 citation statements)

References 26 publications

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“…Guinea pigs respond to AFB 1 with minimal acute multifocal nephrosis of the renal tubules. This is only present following exposure to the LD 50 dose (Netke et al, 1997).…”

Section: Pathologymentioning

confidence: 98%

“…Of the common laboratory species, the guinea pig is one of the most sensitive to the effects of AFB 1 , with an observed LD 50 of 2 mg/ kg body weight via oral gavage and intraperitoneal administration yields an LD 50 of 1.4 mg/kg (Netke et al, 1997). More recently, exposure to feed containing 3 mg/kg AFB 1 has been shown to be sufficient to cause severe renal damage in chicks (Valdivia et al, 2001).…”

Section: Aflatoxin Bmentioning

confidence: 99%

“…All of the aforementioned renal effects occurred in combination with one or more severe hepatic lesions, including hepatoma and hepatocarcinoma (Rati et al, 1991), centrilobular necrosis, endothelial cell degeneration (Netke et al, 1997), and bile duct proliferation (Morrissey et al, 1987).…”

Section: Pathologymentioning

confidence: 99%

See 2 more Smart Citations

Mycotoxins Affecting the Kidney

O'Brien¹,

Dietrich²

2004

Target Organ Toxicology Series

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“…Guinea pigs respond to AFB 1 with minimal acute multifocal nephrosis of the renal tubules. This is only present following exposure to the LD 50 dose (Netke et al, 1997).…”

Section: Pathologymentioning

confidence: 98%

Section: Aflatoxin Bmentioning

confidence: 99%

See 1 more Smart Citation

Mycotoxins Affecting the Kidney

O'Brien¹,

Dietrich²

2004

Target Organ Toxicology Series

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“…In the direct way, Vit C scavenges free radicals formed (Dawson et al, 1990) or interacts with reduced glutathione (Dudek et al, 2005). As an indirect way, it helps recycling vitamin E, thus, supplying active vitamin E (Netke et al, 1997). …”

Section: Vitamins With Antioxidant Properties: Vitamin E and Vitamin Cmentioning

confidence: 99%

Compounds with Antioxidant Capacity as Potential Tools Against Several Oxidative Stress Related Disorders: Fact or Artifact?

Pérez-Matute¹,

Crujeiras²,

Fernández‐Galilea³

et al. 2012

Oxidative Stress and Diseases

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Oxidative Stress and Diseases 544 reactive species: reactive oxygen species (ROS, thus, oxygen-containing molecules that are highly reactive), reactive chlorine species (RCN) and reactive nitrogen species (RNS). All these reactants contain free radicals as well as nonradicals. Low concentrations of these reactive species are necessary for normal cell redox status, cell function and intracellular signalling (Droge, 2002;Valko et al., 2007;Perez-Matute et al., 2009). However, in some disease states, free radicals are produced in excess and can damage DNA, proteins, carbohydrates and lipid constituents and compromise cell function leading to the development of type 2 diabetes, atherosclerosis, obesity, arthritis etc. Thus, it is clear that excessive production of free radicals causes damage to biological material and is an essential event in the aetiopathogenesis of various diseases. However, the question that has risen in the past years is whether uncontrolled formation of ROS is a primary cause or a downstream consequence of the pathological processes. In other words, it is still not clear what comes first, the chicken or the egg. However, what is clear is that there must be a balance between these reactive species and the antioxidants, whose main function is to counteract the deleterious effects of these reactive species. In fact, antioxidant is defined as any substance that when present at low concentrations compared with those of an oxidizable substrate, significantly delays or prevents oxidation of that substrate (Halliwell & Gutteridge, 1999). These defences include both enzymatic (superoxide dismutases, glutathione peroxidase, catalase, thioredoxin) and non-enzimatic systems (vitamins such as vitamin C, E, A, minerals such as selenium, zinc, cooper, bilirrubine, uric acid, some aminoacids etc).Several studies have demonstrated an increased oxidative state (either caused by an increased ROS production or diminished levels of antioxidants) in serious pathologies such as obesity, cardiovascular diseases, metabolic syndrome, cancer etc. Thus, oxidative stress actually may be related with the mentioned processes. In this context, it is tempting to suggest that if oxidative damage significantly contributes to disease pathology, then, actions that decrease it (via decreasing ROS production or increasing endogenous levels of antioxidants) might be therapeutically beneficial. In fact, attenuation or complete suppression of oxidative stress as a way to improve several diseases has flourished as one of the main challenges of research in the last years. Thus, several approaches have been carried out in order to either decrease the high levels of ROS generated or boost the endogenous levels of antioxiants. Inhibition of ROS production through the development of inhibitors (natural or chemical) against the main sources of ROS generation offers an interesting approach. Thus, NADPH oxidase and mitochondria have been postulated as the main targets to reduce ROS production (reviewed by Pérez-Matute et al., 2009). Another str...

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“…Concentrations of ROS are kept under strict control by the activity of innate defense systems including enzymes and non-enzymatic anti-oxidants such as vitamins (Kovacic and Somanathan, 2008). Vitamin C protects cellular membrane lipoproteins against oxidative damage caused by toxic free radicals (Netke et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Effects of vitamin C on inhalation anesthetic isoflurane-induced developmental, neuronal apoptosis in neonatal rats

Shuai

Wang

Xiong

et al. 2014

Bangladesh J Pharmacol

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Research ArticleEffects of vitamin C on inhalation anesthetic isoflurane-induced developmental, neuronal apoptosis in neonatal rats BJP IntroductionAbout 200 million patients worldwide are exposed to anesthesia and undergo surgery each year (Weiser et al., 2008;Moonesinghe et al., 2011). Volatile anesthetics such as isoflurane and sevoflurane are used in millions of young children each year during surgical procedures and imaging studies (Istaphanous and Loepke, 2009). Exposure to anesthetic cocktails (Yon et al., 2005;Lu et al., 2006;Sanders et al., 2009) or volatile agents such as isoflurane even as a single anesthetic (Yon et al., 2005;Ma et al., 2007) has been reported to be associated with widespread apoptotic neurodegeneration in the developing brains and contributes to the post-operative cognitive dysfunction (POCD) (Jevtovic-Todorovic et al., 2003;Satomoto et al., 2009;Brambrink et al., 2010;Kong et al., 2011;Paule et al., 2011; Li et al., 2013a,b).In rodent models, the effects of anesthesia have been evaluated following exposure during a time of peak brain development and synaptogenesis, typically at postnatal day 7 (P7) (Jevtovic-Todorovic et al., 2003;Stratmann et al., 2009b;Shih et al., 2012). Apoptosis has been observed to occur acutely in the period immediately following anesthesia (Jevtovic-Todorovic et al., 2003;Istaphanous et al., 2011;Shih et al., 2012), and the thalamus and hippocampus are known areas susceptible to extensive neurodegeneration (JevtovicTodorovic et al., 2003;Satomoto et al., 2009;Shih et al., 2012). AbstractDevelopmental abnormalities, neuronal apoptosis and associated cognitive impairment following isoflurane exposure in neonatal rodents have been reported. The study was undertaken to investigate the effect of vitamin C supplementation against isoflurane-induced neurotoxicity. Seven day old rats were exposed to 1.1% isoflurane, or air for 6 hours. Treatment groups were administered with vitamin C (30 mg/kg, orally) from postnatal day 1 (P1) to P10 and were exposed to isoflurane on P7. Isoflurane exposure induced apoptosis was determined by Fluoro-Jade C and terminal deoxynucleotidyltransferase-mediated 2'-deoxyuridine 5'-triphosphate nick-end labeling assay. Vitamin C considerably improved memory and learning impairments, modulated neuroapoptosis and improved expressions of brain-derived neurotrophic factor, nerve growth factor, Bcl-xL and decreased activated caspase-3 expressions. Thus, vitamin C effectively offered protection against isoflurane-induced neuronal apoptosis, learning and memory disturbances. Article Info

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Ascorbic Acid Protects Guinea Pigs from Acute Aflatoxin Toxicity

Cited by 57 publications

References 26 publications

Mycotoxins Affecting the Kidney

Mycotoxins Affecting the Kidney

Compounds with Antioxidant Capacity as Potential Tools Against Several Oxidative Stress Related Disorders: Fact or Artifact?

Effects of vitamin C on inhalation anesthetic isoflurane-induced developmental, neuronal apoptosis in neonatal rats

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