Limits...
How much should we involve genetic and environmental factors in the risk assessment of mycotoxins in humans?

Creppy EE, Moukha S, Bacha H, Carratu MR - Int J Environ Res Public Health (2005)

Bottom Line: Within the same range of toxins concentrations in the blood some people develop a disease while others do not.Persons with such haplotype were found to bear chronic interstitial nephropathy with tubular karyomegalic cells while others were apparently healthy.Godin et al. (1996) in France have also found in sibling (a sister and her brother from urban area) that have similar HLA haplotype B35-patern, OTA-related renal tubulopathy with mild proteinuria including beta2-microglobulinuria.

View Article: PubMed Central - PubMed

Affiliation: Dept of Toxicology, University of Bordeaux 2, 146, rue Lóo-Saignat, 33076 Bordeaux, France. edmond.creppy@tox.u-bordeaux2.fr

ABSTRACT
Despite consented efforts in prevention, mycotoxins remain a problem of human health concern in several parts of the world including developed countries. Within the same range of toxins concentrations in the blood some people develop a disease while others do not. Could this inequality in front of mycotoxins effects be explained by environment factors and/or genetic predisposition? Among recent advances in environmental health research Correlation between chronic diseases and mycotoxins in humans deserves attention through several questions: Are genetic factors involved in disease causation of mycotoxins? How much are these factors currently taken into account for mycotoxins risk assessment and how much should we involve them? Answers are still to come. Genetic and environment factors deserve therefore more attention when dealing with regulatory limits, since among the general population, those who are at risk and will develop specific diseases are likely those bearing genetic predispositions. We have addressed these questions for the specific case of ochratoxin A in humans by investigating in Tunisia, county of Jelma, in four rural families forming a household of 21 persons all exposed to ochratoxin A in diet. Our results confirm that ochratoxin A induces chronic tubular nephropathy in humans and mainly point at those having the HLA haplotype A3, B27/35, DR7 to be more sensitive to the disease for quantitatively similar or lower exposure. Persons with such haplotype were found to bear chronic interstitial nephropathy with tubular karyomegalic cells while others were apparently healthy. Godin et al. (1996) in France have also found in sibling (a sister and her brother from urban area) that have similar HLA haplotype B35-patern, OTA-related renal tubulopathy with mild proteinuria including beta2-microglobulinuria. Several mechanisms are discussed that could be put ahead to explain how the HLA haplotype could lead to tubular cells lyses and renal failure. In the mean time it is urgent to search for mass screening biomarkers for mycotoxins in humans and related genetic factors to set-up more appropriate regulation.

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Related in: MedlinePlus

Structure of ochratoxin A
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f1-ijerph-02-00186: Structure of ochratoxin A

Mentions: Taking as example the case of human intake of ochratoxin A in which it is obvious that not all heavily exposed persons are ill, the implication of genetic pre disposition has been investigated in Tunisia (specially the county of Jelma) that is known to be a high spot of OTA exposure in Northern Africa. Ochratoxin A (OTA) (Fig. 1) is produced by several species of fungal genera [1] that is widespread in human food, animal feed and detected in blood and tissues in Tunisia as well as in the Balkans. This mycotoxin has several adverse effects the most prominent being nephrotoxicity and carcinogenicity [2–3, 7, 9].


How much should we involve genetic and environmental factors in the risk assessment of mycotoxins in humans?

Creppy EE, Moukha S, Bacha H, Carratu MR - Int J Environ Res Public Health (2005)

Structure of ochratoxin A
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3814714&req=5

f1-ijerph-02-00186: Structure of ochratoxin A
Mentions: Taking as example the case of human intake of ochratoxin A in which it is obvious that not all heavily exposed persons are ill, the implication of genetic pre disposition has been investigated in Tunisia (specially the county of Jelma) that is known to be a high spot of OTA exposure in Northern Africa. Ochratoxin A (OTA) (Fig. 1) is produced by several species of fungal genera [1] that is widespread in human food, animal feed and detected in blood and tissues in Tunisia as well as in the Balkans. This mycotoxin has several adverse effects the most prominent being nephrotoxicity and carcinogenicity [2–3, 7, 9].

Bottom Line: Within the same range of toxins concentrations in the blood some people develop a disease while others do not.Persons with such haplotype were found to bear chronic interstitial nephropathy with tubular karyomegalic cells while others were apparently healthy.Godin et al. (1996) in France have also found in sibling (a sister and her brother from urban area) that have similar HLA haplotype B35-patern, OTA-related renal tubulopathy with mild proteinuria including beta2-microglobulinuria.

View Article: PubMed Central - PubMed

Affiliation: Dept of Toxicology, University of Bordeaux 2, 146, rue Lóo-Saignat, 33076 Bordeaux, France. edmond.creppy@tox.u-bordeaux2.fr

ABSTRACT
Despite consented efforts in prevention, mycotoxins remain a problem of human health concern in several parts of the world including developed countries. Within the same range of toxins concentrations in the blood some people develop a disease while others do not. Could this inequality in front of mycotoxins effects be explained by environment factors and/or genetic predisposition? Among recent advances in environmental health research Correlation between chronic diseases and mycotoxins in humans deserves attention through several questions: Are genetic factors involved in disease causation of mycotoxins? How much are these factors currently taken into account for mycotoxins risk assessment and how much should we involve them? Answers are still to come. Genetic and environment factors deserve therefore more attention when dealing with regulatory limits, since among the general population, those who are at risk and will develop specific diseases are likely those bearing genetic predispositions. We have addressed these questions for the specific case of ochratoxin A in humans by investigating in Tunisia, county of Jelma, in four rural families forming a household of 21 persons all exposed to ochratoxin A in diet. Our results confirm that ochratoxin A induces chronic tubular nephropathy in humans and mainly point at those having the HLA haplotype A3, B27/35, DR7 to be more sensitive to the disease for quantitatively similar or lower exposure. Persons with such haplotype were found to bear chronic interstitial nephropathy with tubular karyomegalic cells while others were apparently healthy. Godin et al. (1996) in France have also found in sibling (a sister and her brother from urban area) that have similar HLA haplotype B35-patern, OTA-related renal tubulopathy with mild proteinuria including beta2-microglobulinuria. Several mechanisms are discussed that could be put ahead to explain how the HLA haplotype could lead to tubular cells lyses and renal failure. In the mean time it is urgent to search for mass screening biomarkers for mycotoxins in humans and related genetic factors to set-up more appropriate regulation.

Show MeSH
Related in: MedlinePlus