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Citrinin
Citrinin is a mycotoxin which is often found in food. It is a secondary metabolite produced by fungi that contaminates long-stored food and it can cause a variety of toxic effects, including kidney, liver and cell damage. Citrinin is mainly found in stored grains, but sometimes also in fruits and other plant products.
Citrinin was one of the many mycotoxins discovered by H. Raistrick and A.C. Hetherington in the 1930s. In 1941 H. Raistrick and G. Smith identified citrinin to have a broad antibacterial activity. After this discovery the interest in citrinin rose. However, in 1946 A.M. Ambrose and F. DeEds demonstrated that citrinin was toxic to mammals. As a result, the interest in citrinin decreased, but there still was a lot of research.[specify] In 1948 the chemical structure was found by W.B. Whalley and coworkers. Citrinin is a natural compound and it was first isolated from Penicillium citrinum, but is also produced by other Penicillium species, such as the Monascus species and the Aspergillus species, which are both fungi. During the 1950s W.B. Whalley, A.J. Birch and others identified citrinin as a polyketide and investigated its biosynthesis using radioisotopes.[specify] During the 1980s and 1990s J. Staunton, U. Sankawa and others also investigated its biosynthesis using stable isotopes and NMR. The gene cluster expression system for citrinin was reported in 2008.
In 1993 the World Health Organisation International Agency for Research on Cancer started to evaluate the carcinogenic potential of mycotoxins. The health hazards of mycotoxins to humans or animals have been reviewed extensively in recent years. To ensure agricultural productivity and sustainability, animal and public health, animal welfare and the environment, maximum levels of undesirable substances in animal feed are laid down in the EU Directive of the European Parliament and the Council of 7 May 2002. While maximum levels for various mycotoxins were set for a number of food and feed products, the occurrence of citrinin is not regulated yet under these or other regulations within the European Union. No maximum levels have been reported yet by the Food and Agriculture Organization for citrinin in food and feed.
Citrinin is a polyketide mycotoxin, which is a secondary metabolite of some fungi species. Its IUPAC name is (3R,4S)-4,6-dihydro-8-hydroxy-3,4,5-trimethyl-6-oxo-3H-2-benzopyran-7-carboxylic acid and the molecular formula is C13H14O5. Citrinin has a molecular weight of 250.25 g/mol. It forms disordered yellow crystals which melt at 175 °C. Citrinin is a planar molecule which contains conjugated bonds. As a result of these conjugated bonds citrinin is autofluorescent. Citrinin crystals can hardly be dissolved in cold water, however in polar organic solvents and aqueous sodium hydroxide, sodium carbonate and sodium acetate dissolving is possible.
As stated above, citrinin decomposes at temperatures higher than 175 °C, providing that it is under dry conditions. When water is present, the decomposition temperature is around 100 °C. Several decomposition products of citrinin are known, including phenol A, citrinin H1, citrinin H2 and dicitrinin A. The structures of the decomposition products are shown in figure 1, depicted on the left. Citrinin H1 is produced out of two citrinin molecules and its toxicity is increased compared to the original toxicity of citrinin. Citrinin H2, a formylated derivative of phenol A, is less toxic than citrinin. Phenol A seems to be produced mainly under acidic conditions. Dicitrinin A is a dimer of citrinin molecules which is mainly formed during decomposition in a neutral environment, when a high concentration of citrinin is present.
The way citrinin reacts in the body is not understood yet and its intermediates during biotransformation are also not known.
Citrinin often occurs together with other mycotoxins like ochratoxin A or aflatoxin B1, because they are produced by the same fungi species. The combination which is observed most often is citrinin with ochratoxin A and this is also the most studied combination. The effects of co-occurrence of these mycotoxins are either additive or synergistic. The nephrotoxic effects of ochratoxin A and citrinin, for example, are increased synergistic when exposure to both takes place. Next to that, the co-exposure of these compounds is expected to be involved in the pathogenesis of a human kidney disease, called Balkan Endemic Nephropathy. The interaction of both substances might also influence apoptosis and necrosis in hepatocytes.
The existing information on occurrence of citrinin in food suggests that relatively high citrinin concentrations can be found in stored grains and grain-based products. Because of this and the fact that people in general have a high consumption of cereal-based foods, the Panel on Contaminants in the Food Chain (the CONTAM Panel) considered that grains might be the major contributor of dietary exposure to citrinin. The CONTAM Panel concluded that not enough data were available in the literature to carry out a dietary exposure assessment.
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Citrinin
Citrinin is a mycotoxin which is often found in food. It is a secondary metabolite produced by fungi that contaminates long-stored food and it can cause a variety of toxic effects, including kidney, liver and cell damage. Citrinin is mainly found in stored grains, but sometimes also in fruits and other plant products.
Citrinin was one of the many mycotoxins discovered by H. Raistrick and A.C. Hetherington in the 1930s. In 1941 H. Raistrick and G. Smith identified citrinin to have a broad antibacterial activity. After this discovery the interest in citrinin rose. However, in 1946 A.M. Ambrose and F. DeEds demonstrated that citrinin was toxic to mammals. As a result, the interest in citrinin decreased, but there still was a lot of research.[specify] In 1948 the chemical structure was found by W.B. Whalley and coworkers. Citrinin is a natural compound and it was first isolated from Penicillium citrinum, but is also produced by other Penicillium species, such as the Monascus species and the Aspergillus species, which are both fungi. During the 1950s W.B. Whalley, A.J. Birch and others identified citrinin as a polyketide and investigated its biosynthesis using radioisotopes.[specify] During the 1980s and 1990s J. Staunton, U. Sankawa and others also investigated its biosynthesis using stable isotopes and NMR. The gene cluster expression system for citrinin was reported in 2008.
In 1993 the World Health Organisation International Agency for Research on Cancer started to evaluate the carcinogenic potential of mycotoxins. The health hazards of mycotoxins to humans or animals have been reviewed extensively in recent years. To ensure agricultural productivity and sustainability, animal and public health, animal welfare and the environment, maximum levels of undesirable substances in animal feed are laid down in the EU Directive of the European Parliament and the Council of 7 May 2002. While maximum levels for various mycotoxins were set for a number of food and feed products, the occurrence of citrinin is not regulated yet under these or other regulations within the European Union. No maximum levels have been reported yet by the Food and Agriculture Organization for citrinin in food and feed.
Citrinin is a polyketide mycotoxin, which is a secondary metabolite of some fungi species. Its IUPAC name is (3R,4S)-4,6-dihydro-8-hydroxy-3,4,5-trimethyl-6-oxo-3H-2-benzopyran-7-carboxylic acid and the molecular formula is C13H14O5. Citrinin has a molecular weight of 250.25 g/mol. It forms disordered yellow crystals which melt at 175 °C. Citrinin is a planar molecule which contains conjugated bonds. As a result of these conjugated bonds citrinin is autofluorescent. Citrinin crystals can hardly be dissolved in cold water, however in polar organic solvents and aqueous sodium hydroxide, sodium carbonate and sodium acetate dissolving is possible.
As stated above, citrinin decomposes at temperatures higher than 175 °C, providing that it is under dry conditions. When water is present, the decomposition temperature is around 100 °C. Several decomposition products of citrinin are known, including phenol A, citrinin H1, citrinin H2 and dicitrinin A. The structures of the decomposition products are shown in figure 1, depicted on the left. Citrinin H1 is produced out of two citrinin molecules and its toxicity is increased compared to the original toxicity of citrinin. Citrinin H2, a formylated derivative of phenol A, is less toxic than citrinin. Phenol A seems to be produced mainly under acidic conditions. Dicitrinin A is a dimer of citrinin molecules which is mainly formed during decomposition in a neutral environment, when a high concentration of citrinin is present.
The way citrinin reacts in the body is not understood yet and its intermediates during biotransformation are also not known.
Citrinin often occurs together with other mycotoxins like ochratoxin A or aflatoxin B1, because they are produced by the same fungi species. The combination which is observed most often is citrinin with ochratoxin A and this is also the most studied combination. The effects of co-occurrence of these mycotoxins are either additive or synergistic. The nephrotoxic effects of ochratoxin A and citrinin, for example, are increased synergistic when exposure to both takes place. Next to that, the co-exposure of these compounds is expected to be involved in the pathogenesis of a human kidney disease, called Balkan Endemic Nephropathy. The interaction of both substances might also influence apoptosis and necrosis in hepatocytes.
The existing information on occurrence of citrinin in food suggests that relatively high citrinin concentrations can be found in stored grains and grain-based products. Because of this and the fact that people in general have a high consumption of cereal-based foods, the Panel on Contaminants in the Food Chain (the CONTAM Panel) considered that grains might be the major contributor of dietary exposure to citrinin. The CONTAM Panel concluded that not enough data were available in the literature to carry out a dietary exposure assessment.