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Toxic Effects of Citrinin in Animals and Poultry

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Toxic Effects of Citrinin in Animals and Poultry Vol.5 No.4 April-June 2018 ISSN: 2321-6387 Toxic Effects of Citrinin in Animals and Poultry D.Basheer Ahamad Department of Veterinary Pathology, Veterinary College and Research Institute, Tamil Nadu Veterinary and Animal Sciences University, Tirunelveli, Tamil Nadu, India Article Received on 20.03.2018 Article Published on 19.04.2018 Introduction and Aspergillus oryzae, the latter being Citrinin (CTN) is a secondary used to produce sake, miso, and soy sauce product of fungal metabolism, first isolated (Manabe, 2001). by Hetherington and Raistrick from a Citrinin is nephrotoxic and culture of Penicillium citrinum Thom implicated in disease outbreaks in both (Hetherington and Raistrick, 1931). animals and humans. Acutely lethal doses Meanwhile, several other fungal species administered to rabbits, guinea pigs, rats, within the three genera, Penicillium (P. swine, or mice caused swelling of the expansum, P. verrucosum), Aspergillus (A. kidneys with eventual necrosis (Friss et al., terreus), and Monascus (M. ruber) were 1969; Jordan et al., 1978; Krogh, 1978, also found to produce this mycotoxin Krogh et al., 1974). In mice, citrinin is (Ciegler et al., 1977, Bragulat et al., 1977). also embryocidal and fetotoxic (Hood et CTN contaminates maize (Nelson et al., al., 1976). In rats, citrinin has similar 1985), wheat, rye, barley, oats (Scott et effects and high doses are teratogenic al.,1972), and rice (Tanaka et al., 2007). (Reddy et al., 1982a,b). Citrinin has been Citrinin was considered as a potential implicated in porcine and avian antibiotic (IARC, 1986), but its toxic nephropathies and possibly in the fatal properties prevented its therapeutic use. renal disease in humans, causing endemic Citrinin (CTN), a low molecular weight Balkan nephropathy (Friss et al., 1969;, compound, that melts at 172oC and is Krogh et al., 1970 Witlock, et al., 1977). soluble in dilute sodium hydroxide, The nephropathy of citrinin in rats was sodium carbonate, methanol, ethanol and characterized by an enhanced excretion of other polar solvents (Leatherhead Food dilute urine glucosuria, proteinuria, and Research, 2000) was first isolated as a reduced glomerular filtration rate and renal pure compound from a culture of blood flow (Petkova-Bocharova et al., Penicillium citrinum in 1931. Later, 1991). yellowish coloured rice imported from The kidney is the major target Thailand to Japan in 1951 was found to be organ of CTN toxicity, but other target contaminated with citrinin. Subsequently, organs such as liver and bone marrow it was identified in over a dozen species of (Gupta et al., 1983). CTN could be Penicillium including certain strains of implicated in porcine nephropathy (Krogh Penicillium camemberti (used to produce et al., 1973). It is frequently found in food cheese) and several species of Aspergillus and feed in combination with ochratoxin A ( Aspergillus terreus, Aspergillus niveus) (OTA), and these two nephrotoxic Shanlax International Journal of Veterinary Science 12 Vol.5 No.4 April-June 2018 ISSN: 2321-6387 mycotoxins are suspected to be involved in positive for CTN in the range of 3-70 ppb. the aetiology of a human kidney disease An outbreak of pruritis, pyrexia and called Balkan endemic nephropathy. In the haemorrhagic syndrome in cattle was endemic area in Bulgaria, CTN had higher attributed to feeding of citrus pulp concentrations in maize and beans containing citrinin 30 - 40 ppb (Griffiths intended for human consumption than in and Done, 1991). the non-endemic area (Petkova-Bocharova In India, Pande et al. (1990) et al., 1991). CTN is also found to increase reported the occurrence of CTN in feed. the toxicity of OTA either additively Manickam et al. (1985) encountered (Ahamad et al., 2006) or synergistically mycotoxicosis in buffaloes due to (Speijers and Speijers, 2004). The ingestion of mouldy fodder contaminated International Agency for Cancer Research with AFB1, CTN, ochratoxin and (IARC) classified CTN in Group 3 of penicillic acid of which CTN alone was carcinogens because of the limited present in around 18 per cent of samples. evidence of its carcinogenicity to Sundaram et al. (1999) recorded the co- experimental animals and no evidence for occurrence of CTN and AFB1 in maize. humans (IARC, 1986). Citrinin affects the Out of 229 samples of maize tested, 45 animals in a number of ways i.e. it leads to were positive for CTN, of which 23 decreased body weight, immunotoxicity, samples also contained AFB1. Natural nephrotoxicity, hepatotoxicity, occurrence of citrinin has been reported in teratogeniccity. Oxidative stress, apoptosis various agricultural products like coconut were found to be the important mechanism (Kumari and Nusrath, 1987), rice (Reddy for causing these effects and Reddy., 1983;, cereals (Pande et al., 1990), some herbal medicinal plants (0.01 Incidence of Citrinin - 0.76mg/ g) (Roy and Kumari, 1991; Krogh et al. (1973) reported Chourasia, 1995), groundnut ochratoxin A and CTN in cereals with an (Subrahmanyam and Rao, 1974; Mehan incidence of 58 and 9 per cent, and McDonald, 1984), sesame (Reddy and respectively, and these mycotoxins were Reddy, 1983), bakery bread (Sinha et al., also implicated in porcine nephropathy in 1994), poultry feeds (Rajeswari and Char, Denmark. Reiss (1977) considered CTN 1991), milk and milk products (Singh et responsible for “yellowed rice syndrome”, al., 1992), cattle feed (Jeswal and Jeswal, an animal mycotoxicosis in Japan. 1990; Ranjan and Sinha, 1991), root drugs Yoshisawa (1991) observed natural (Roy and chourasia, 1990) and dry fruits ( contamination of CTN in corn, rice, rye, Saxena et al., 1988). Ahamad and wheat, barley, oats and decaying tomato Vairamuthu (2000) recorded up to 400 ppb fruits. Abdelhamid (1990) reported the of CTN when singly or combination with occurrence of various mycotoxins in aflatoxin B1 (AFB1); up to 4800 ppb of Egyptian feeds in which 44.2 per cent of CTN in combination with ochratoxin A feed samples tested were positive for (OTA) up to 320 ppb of CTN in aflatoxin (AF) containing less than 100 combination with CTN- AFB1- OTA in ppb, and 15.4 per cent of samples were poultry feed where as CTN alone up to Shanlax International Journal of Veterinary Science 13 Vol.5 No.4 April-June 2018 ISSN: 2321-6387 1800 ppb; CTN with AFB1 up to 400 ppb, effect has been reported from pigs given CTN with OTA up to 600 ppb and up to 20 µg/kg b.w. per day (Sándor et al., 1200 of CTN when combination of CTN, 1991). AFB1-OTA in feed ingredients such as maize, sorghum, jowar, soya meal, sun Dogs flower oil cake and groundnut oil cake. In an early study, dogs were given citrinin with 5 mg/kg b.w. i.p. survived the Toxic Effects of Citrinin in Animals entire study, but severe proximal tubule Pigs damage was observed during the post- A case study by Friis et al. (1969) mortem examination. (Kitchen et al., reported the results from pigs administered 1977a, b, c). Anorexia, emaciation, citrinin in feed at 20, 40 or 100 mg/kg b.w. vomiting and polydipsia/polyuria and per day. At the highest dose level, the pigs consumption of the feed was reported to be died in a coma with renal insufficiency and „over one month‟. The dogs had high a decrease in appetite was observed in all blood urea nitrogen and creatinine. Two animals. At 20 and 40 mg/kg b.w. per day severely affected dogs died, while the growth depression, loss of weight and others recovered gradually. Renal failure, glucosuria were observed. The data are with renal atrophy, congestion of the poorly reported and as such were not used glomerula capillary, and diffuse for risk assessment. Sándor et al. (1991) degeneration, necrosis, dystrophic described a subacute toxicity study with calcification and regeneration of the ochratoxin A and citrinin in swine. Pigs tubular epithelium were seen @citrinin at are able to tolerate citrinin concentrations 8.3 µg/kg feed (Ahn et al., 2007) and in feed resulting in doses of up to 0.02 severe scrotal dermatitis 150 µg citrinin/kg mg/kg b.w. per day for a longer period feed (Little et al., 1991). without any signs of toxicity. Szczech et al. (1974) reported increased Toxic Effects of Citrinin in concentrations of glutamic oxalacetic Experimental Animals transaminase, isocitric dehydrogenase and Lethal Dose lactic dehydrogenase in serum and urine Acute LD50 of CTN varies with before clinical signs of renal disease were the route of administration, physiological evident in pigs given oral doses of 1.0 and conditions, and animal species Oral LD50 20.0 mg citrinin/kg b.w. per day. The for rats is 50 mg kg-1 b.w. while activities of the enzymes were elevated in subcutaneous LD50 is 67 mg kg-1 b.w. urine, whilst no other signs of renal (Ambrose and DeEds, 1945). In the Dutch disease were observable, and there was no Belted rabbit, oral LD50 is 134 mg kg-1, alteration in blood urea nitrogen. An early and in the New Zealand White rabbit it is elevation in these serum activities is about 120 mg kg-1 (Hanika et al., 1983, acknowledged to be a sensitive indicator Hanika et al., 1984). The LD50 of CTN for of renal damage. In conclusion, only few ducks is 57 mg/kg, for a rat 60mg/kg, for studies on adverse effects of citrinin in chickens 95 mg/kg, and for rabbits 134 pigs could be identified. At present, no mg/kg (Hanika et al., 1983). In a LD50 Shanlax International Journal of Veterinary Science 14 Vol.5 No.4 April-June 2018 ISSN: 2321-6387 study with hamsters, citrinin caused slight aminotransferase (AST) and Lactate to mild necrosis of scattered individual dehydrogenase (LDH) in rats (Beasley et lymphocytes in the spleen and the al., 1986; Singh et al., 2006).
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