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Associated efficiency of Saccharomyces cerevisiae and vitamin E in ameliorating adverse effects of ochratoxin A on production performance in broiler chickens

Published: July 25, 2019
By: Satyendra Singh 1, Ram Singh 2, A. B. Mandal 3 and Mohit Singh 4. / ICAR-Central Avian Research Institute, Izatnagar, Uttar Pradesh 243 122 India.
Summary

In the present study, efficiency of Saccharomyces cerevisiae and vitamin E together in ameliorating ochratoxicosis in broiler chickens was investigated. Day-old broiler chicks (320) were divided into 8 treatment groups (T1- control (basal diet); T2- T1+ 150 ppb OTA; T3-T2 + 0.05% SC + 100 mg vitamin E-VE; T4- T2 + 0.075% SC + 100 mg VE; T5- T2 + 0.1% SC + 100 mg VE; T6- T2 + 0.05% SC + 200 mg VE; T7- T2 + 0.075% SC + 200 mg VE; T8- T2 + 0.1% SC + 200 mg VE per kg diet). Each diet was fed to 5 replicated groups of 8 birds from 0 to 42 days of age. During overall growth period (0–6 weeks), the body weight gain (BWG) of birds fed ochratoxin contaminated diet (T2) was lower than that of control group (T1). The BWG of group T5, T7 and T8 was higher than T2 but statistically similar to that of control. During overall growth period, the FI in control group was statistically similar to other treatment groups. The FI in groups T7 and T8 was higher than that of group received basal diet with toxin (T2). The overall FCR in control group (T1) was lower than that of T2. The FCR in groups T3, T4 and T6 was higher than the control, but lower than that of T2. The FCR in groups T5, T7 and T8 was lower than T2 and statistically similar to that of control (T1). The overall liveability percentage in control group (T1) was higher than that of ochratoxin fed group (T2). The liveability percentage in group T3 was lower than control and similar to that of T2. The liveability percentage in groups T4 to T8 was statistically similar to that of control. Ochratoxin contamination in diet caused significant reduction in body weight gain, feed consumption, feed efficiency and livability percentage. It was concluded that inclusion of S. cerevisiae at 0.1% level along with 100 mg vitamin E per kg diet or S. cerevisiae at 0.075% level along with 200 mg vitamin E/kg diet to the ochratoxin (150 ppb) contaminated feed ameliorated the adverse effects of ochratoxicosis on production performance of broiler chickens.

Key words: Broiler chicken, Ochratoxin, Saccharomyces cerevisiae, Vitamin E.

The presence of ochratoxin A in poultry feed causes significantly to health disorders and decreases production. In a survey conducted to investigate global occurrence of mycotoxins, the incidence of OTA in South Asia was found to be 55% on analyzing the feed samples (Nahrer and Kovalsky 2014). Ochratoxin A causes significant losses and reduction in the profitability of poultry industry due to its effects on performance and health (Agawane and Lonkar 2004). It causes a reduction in productive performance (growth rate, feed consumption, poorer feed conversion) and increased mortality (Singh et al. 2015, Singh et al. 2016). The risk associated with ochratoxin residues in poultry meat represents a public health concern. For preventive management of mycotoxins in the field and during storage, new approaches have been employed including physical, chemical and nutritive treatments that can be advised to detoxify mycotoxins in contaminated feeds and feedstuffs (Varga and Toth 2005) along with amelioration of its toxicity in animal body system. A live yeast, Saccharomyces cerevisiae, was found to alleviate the adverse effects of mycotoxicosis in poultry (Stanley et al. 1993). S. cerevisiae has shown considerable binding ability with several commonly occurring mycotoxins (Devegowda et al. 1998), and is also found more effective as a low inclusion binder to bind mycotoxins present in contaminated poultry feed when compared with other physical or chemical materials (Mahesh and Devegowda 1996). Incorporation of 0.1% S. cerevisiae to the ochratoxin contaminated diet ameliorated the ill effects of ochratoxicosis as evidenced through production performance and relative weight of organs during 0–6 weeks of age in broiler chickens (Singh et al. 2016). Various antioxidants are beneficial in reducing the toxicity of ochratoxins, involved in increasing oxidative stress (Sorrenti et al. 2013). Vitamin C and E, being antioxidants, play an important role in the stimulation and enhancement of the chicken immune response.The objective of this investigation was to study the associated efficiency of S. cerevisiae and vitamin E to ameliorate ochratoxicosis in broiler chickens.
MATERIALS AND METHODS
Ochratoxin production:The lyophilised preparation of Aspergillus westerdijkiae NRRL 3147 was revived on potato dextrose agar medium and used for experimentation. Ochratoxin was produced as per Singh et al. (2013). Cracked maize (50 g) was taken in 250 ml conical flasks. The moisture content of substrate was adjusted to have a moisture level of 35%. Thus flasks were plugged with nonabsorbent cotton and sealed with aluminium foil. The flasks were autoclaved for 20 min at 121°C and inoculated with 1-week old mycelium of Aspergillus westerdijkiae NRRL 3174. The inoculated flasks were incubated in a BOD incubator for 14 days. After removal from the incubator, the flasks were dried at 70°C and the ochratoxin assays were performed as per AOAC (1995).
Experimental design: Experimental design was completely randomized design (CRD). There were 8 dietary treatments. Each dietary treatment had 5 replicates and each replicate had 8 chicks. The experiment was conducted in broiler chickens from day-old to 6 weeks of age. The various dietary treatments were prepared by mixing the required quantity of mouldy maize to get the desired concentration of 150 ppb OTA in basal diet (Table 1).
Associated efficiency of Saccharomyces cerevisiae and vitamin E in ameliorating adverse effects of ochratoxin A on production performance in broiler chickens - Image 1
Biological experiment and analysis: Day-old broiler chicks (320) were obtained from experimental hatchery, CARI, Izatnagar. The chicks were wing banded, weighed individually and distributed randomly into 8 groups. All birds were reared under standard management conditions from 0–6 weeks. All birds were fed with broiler starter ration from 1–21 days and broiler finisher ration from 22 to 42 days. The ingredient and chemical composition of broiler starter and finisher ration are presented in Table 2.
Associated efficiency of Saccharomyces cerevisiae and vitamin E in ameliorating adverse effects of ochratoxin A on production performance in broiler chickens - Image 2
The protein as per AOAC (1995) and calcium contents as per Talapatra et al. (1940) were estimated, while the concentrations of lysine, methionine, available P and metabolizable energy values were calculated. Weekly individual body weight and feed consumption of each group were recorded and the FCR was calculated. Mortality was recorded as and when occurred. The statistical analysis was done using SPSS 16.0 version.
RESULTS AND DISCUSSION
The data pertaining to body weight gain (BWG), feed intake (FI) and feed conversion ratio (FCR) at different growth phases is presented in Table 3.
Associated efficiency of Saccharomyces cerevisiae and vitamin E in ameliorating adverse effects of ochratoxin A on production performance in broiler chickens - Image 3
Body weight gain (BWG):Significant (P≤0.05) difference in BWG among various dietary treatments were recorded from second week of age onwards. During starting growth phase (0–3 weeks), the BWG of birds in control group (T1) was higher (P≤0.05) than that of ochratoxin fed group (T2). The BWG in T3 and T4 was lower (P≤0.05) than control but higher (P≤0.05) than that of toxin fed group (T2). However, the BWG in T5 was statistically similar to that of control, indicating that addition of 0.1% S. cerevisiae along with 100 mg vitamin E to the ochratoxin contaminated diet ameliorated the adverse effects of ochratoxicosis. The BWG of T6 was lower (P≤0.05) than control, but higher (P≤0.05) than that of toxin (T2) fed group. The BWG in groups T7 and T8 was higher (P≤0.05) than T2 and statistically similar to that of control, depicting that addition of 0.075% S. cerevisiae along with 200 mg vitamin E (T7) was efficient to ameliorate the adverse effects of ochratoxicosis during starting growth phase. During finisher phase (4–6 weeks), the BWG in control group was higher (P≤0.05) than that of toxin fed group (T2). The BWG in T3 to T8 was statistically similar to that of control. During overall growth period (0–6 weeks), the BWG of control group (T1) was higher (P≤0.05) than that of toxin fed group (T2). The BWG of groups T3, T4 and T6 did not vary (P≤0.05) from that of toxin fed group (T2). The BWG of group T5, T7 and T8 was higher (P≤0.05) than T2 but statistically similar to that of control, indicating that addition of S. cerevisiae along with vitamin E to the ochratoxin contaminated diet ameliorated the adverse effects of ochratoxicosis in groups T5, T7 and T8.
The present investigation indicated that addition of 150 ppb ochratoxin to the basal diet of broiler chickens resulted in significant decrease in body weight gain of broilers. Significant reduction in BWG of birds was in agreement with previous investigation with dietary ochratoxin level of 50–100 ppb (Stove et al. 2004, El-Barkouky 2008, ElBarkouky and Abu- Taleb 2008), 200 ppb (Sakhareet al. 2007, El-Barkouky et al. 2010, Singh et al. 2015, Singh et al. 2016) and 567 ppb (Garcia et al. 2003). In the present study, inclusion of 0.1% S. cerevisiae + 100 mg vitamin E or 0.075% S. cerevisiae + 200 mg vitamin E per kg to the ochratoxin contaminated feed ameliorated the adverse effects of ochratoxin on weight gain of broiler chickens. El-Barkouky (2008) and El-Barkouky et al. (2010) also reported that addition of S. cerevisiae to broiler diet provided partial protection against ill effects of ochratoxin on growth. Stanley et al. (1993), Mahesh and Devegowda (1996), Volkl and Karlovsky (1998) found that S. cerevisiae has beneficial effects on weight gain of broiler chickens exposed to mycotoxins. Singh et al. (2016) reported that incorporation of 0.1% S. cerevisiae to the ochratoxin contaminated diet ameliorated the ill effects of ochratoxicosis on production performance and relative weight of organs in broiler chickens. S. cerevisiae has considerable binding ability against ochratoxin (Devegowda et al. 1998) and protect the birds against its harmhul effects. Also, Singh (2015) reported that addition of 200 mg/kg vitamin E to the 200 ppb ochratoxin contaminated feed ameliorated the adverse effects of ochratoxicosis.
Decreased body weight gain might be attributed to the decrease in protein absorption and/or utilization or to the inhibition of protein synthesis caused by ochratoxin (Kubena et al. 1983, 1988 and 1989). The amelioration of ochratoxicosis on addition of S. cerevisiae might be attributed to its adsorption ability as reported by several workers. Several studies indicated involvement of oxidative stress to the toxicity of ochratoxin (Baudrimont et al. 1994, Omar et al. 1998, Rahimtula et al. 1988). Rahimtula et al. (1988) reported that ochratoxin induced lipid peroxidation (LPO) in subcellular fractions. There is also evidence showing that ochratoxin is a potent pro-oxidant as it induced LPO in primary cultures of brain cells (Belmadani et al. 1999). In addition, the formation of reactive oxygen species (ROS) was significantly increased after exposure of foetal rat telencephalon cells to high ochratoxin concentrations (Monnet-Tschudi et al. 1997). The kidney is a prominent site for intense oxidative processes in the body and ROS plays an important role in the pathogenesis of a variety of renal diseases (Shiraishi et al. 2000). Therefore, supplementation of vitamin E might have reduced the oxidative stress caused by ochratoxin and thus cell damage.
Feed intake (FI):During starter phase (0–3 weeks), the FI in control group (T1) was higher than that of toxin fed group (T2). The FI in groups T3 and T6 was statistically similar to that of T2, however, the FI in groups T4, T5, T6 and T7 was higher than that of T2. During finisher phase (4–6 weeks), FI did not differ (P≤0.05) among various dietary treatments. During overall growth period (0–6 weeks), the FI in control group was statistically similar to other treatment groups. The FI in groups T7 and T8 was higher (P≤0.05) than that of group received basal diet with toxin (T2). In the present study, dietary contamination of ochratoxin resulted in reduced feed consumption in broilers. Similar observations of reduced feed consumption were also reported by earlier workers (Verma et al. 2004, Elaroussi et al. 2006, Denli et al. 2008 and Sawale et al. 2009). Other workers (El-Barkouky 2008, El-Barkouky and Abu- Taleb 2008, El-Barkouky et al. 2010, Singh et al. 2015, Singh et al. 2016), also reported significantly reduced feed intake in broilers fed ochratoxin contaminated feed at a concentration ranging from 50–200 ppb. In the present study, addition of 0.1% S. cerevisiae along with 100 mg vitamin E or 0.075% S. cerevisiae along with 200 mg vitamin E/kg diet to the 150 ppb ochratoxin contaminated feed ameliorated the ill effects of ochratoxin on feed consumption of broilers. El-Barkouky (2008), El-Barkouky et al. (2010) and Singh et al. (2016) also reported that addition of S. cerevisiae to the 50–200 ppb ochratoxin contaminated diet improved the feed consumption in broiler chickens. Also, Singh (2015) reported that addition of vitamin E (200 mg/kg) to 200 ppb ochratoxin contaminated feed ameliorated the adverse effects of ochratoxicosis on feed intake of broiler chickens.
Associated efficiency of Saccharomyces cerevisiae and vitamin E in ameliorating adverse effects of ochratoxin A on production performance in broiler chickens - Image 4
Feed conversion ratio (FCR): With regard to FCR in various growth phases, the FCR during starter phase (0–3 weeks) in control group (T1) was lower (P≤0.05) than that of ochratoxin fed group (T2). The FCR in groups T3 to T7 was higher (P≤0.05) than T1 but lower than that of T2. The FCR of group T8 was statistically similar to that of control. During finisher phase (4–6 weeks) and overall growth phase (0–6 weeks), the FCR in control group (T1) was lower (P≤0.05) than that of T2. The FCR in groups T3, T4 and T6 was higher (P≤0.05) than the control, but lower than that of T2. The FCR in groups T5, T7 and T8 was lower than T2 and statistically similar to that of control (T1), indicating that inclusion of S. cerevisiae along with vitamin E in T5, T7 and T8 ameliorated the adverse effects of ochratoxicosis on FCR. In the present study, ochratoxin (150 ppb) contamination in feed significantly (P≤0.05) increased the FCR, thus resulted in poor feed efficiency in broiler chickens. Poor feed efficiency due to ochratoxin contamination in feed was earlier reported by Elaroussi et al. (2006), Santin et al. (2006), Koynarski et al. (2007), Hanif et al. (2008), Denli et al. (2008) and Sawale et al. (2009). Singh et al. (2016), Sakhare et al. (2007), El-Barkouky (2008), El-Barkouky and Abu-Taleb (2008), El-Barkouky et al. (2010) and Singh et al. (2015) also reported poor feed conversion in broiler chickens fed ochratoxin (50–200 ppb) contaminated feed. The present study revealed that inclusion of S. cerevisiae (0.1%) along with vitamin E (100 mg/kg feed) or S. cerevisiae (0.075%) along with vitamin E (200 mg/kg feed) to the 150 ppb ochratoxin contaminated feed ameliorated the adverse effects of ochratoxicosis on feed efficiency in broiler chickens. El-Barkouky (2008), El-Barkouky et al. (2010) and Singh et al. (2016) also reported that addition of S. cerevisiae in the diet of broiler chickens ameliorated the ill effects of 50–200 ppb ochratoxin on feed efficiency. Singh (2015) also reported that addition of vitamin E at 200 mg/ kg level to 200 ppb ochratoxin contaminated feed ameliorated the adverse effects of ochratoxicosis on feed efficiency in broiler chickens.
Liveability percentage:During first week of age, no mortality was recorded. During second, third and fourth weeks of growth period, the liveability percentage did not vary (P≤0.05) among various dietary treatments. During fifth week of age, the liveability percentage in control group (T1) was higher (P≤0.05) than that of ochratoxin fed group (T2). The liveability percentage in groups T3 to T8 was statistically similar to that of control. During sixth week of growth trial, the liveability percentage in control group (T1) was 95.00 which significantly (P≤0.05) reduced to 82.50 in ochratoxin fed group (T2). The liveability percentage in group T3 was significantly (P≤0.05) lower than control and similar to that of T2. The liveability percentage in groups T4 to T8 was statistically similar to that of control, indicating that inclusion of S. cerevisiae along with vitamin E at any level in these groups ameliorated the adverse effects of ochratoxicosis on mortality in birds. The present study revealed that ochratoxin (150 ppb) contamination of broiler feed resulted in higher mortality compared to that of control. These findings were in agreement with earlier reports in literature (Singh et al. 2016, El-Barkouky and Abu-Taleb 2008, El-Barkouky et al. 2010, Singh et al. 2015). Our results revealed that addition of S. cerevisiae along with vitamin E at any level, barring T3, to the ochratoxin contaminated broiler diet alleviated the adverse effects on mortality caused by ochratoxicosis in broiler chickens. Stanley et al. (1993), El-Barkouky (2008), El-Barkouky et al. (2010) and Singh et al. (2016) also reported that addition of S. cerevisiae in the diet of broiler chickens ameliorated the ill effects of 50–200 ppb ochratoxin on mortality. Singh (2015) also reported that addition of vitamin E at 100 mg/kg level to 200 ppb ochratoxin contaminated feed ameliorated the adverse effects of ochratoxicosis on mortality in broiler chickens.
Cost of feeding:During starter phase (0–3 wk), the feed cost (Table 5) in control group (T1) was lower (P£0.05) that that of T2. The feed cost in groups T3 to T8 was higher (P£0.05) than control (T1) but lower (P£0.05) than that of toxin fed group (T2). During finisher phase (4–6 wk), the feed cost in control group (T1) was lower (P£0.05) that that of T2. The feed cost in groups T5 and T8 was statistically similar to that of control, however, the feed cost in groups T3, T4, T6 and T7 was higher (P£0.05) than that of control. Between T5 and T7, the cost of feed in group T5 was statistically similar to that of control, however, the feed cost in group T7 was higher (P£0.05) than that of control. Therefore, the cost of feeding in group T5 was lower than that of T7. During overall growth period (0–6 wk), the feed cost in control group (T1) was lower (P£0.05) that that of T2 due to depressed growth and feed conversion caused by ochratoxin contamination in T2. The feed cost in groups T3 to T8 was higher (P£0.05) than that of control. Between T5 and T7, the cost of feed in group T5 was lower than that of T7. The results indicated that the feed-cost of production was reduced when additives were added in ochratoxin contaminated diet, attributed to ameliorating effect of those additives on performance. However, the production cost, incurred due to addition of additives, could not be compensated.
Associated efficiency of Saccharomyces cerevisiae and vitamin E in ameliorating adverse effects of ochratoxin A on production performance in broiler chickens - Image 5
It was concluded that ochratoxin contamination of feed at the rate of 150 ppb impaired the production performance assessed through body weight gain, feed intake, feed utilization efficiency and survivability. Inclusion of Saccharomyces cerevisiae at 0.1% level along with 100 mg vitamin E/kg diet or Saccharomyces cerevisiae at 0.075% level along with 200 mg vitamin E/kg diet to the ochratoxin (150 ppb) contaminated feed ameliorated the adverse effects of ochratoxicosis in broiler chickens. However, the production cost, incurred due to addition of additives to ameliorate the adverse effects of ochratoxin could not be compensated.
This article was originally published in Indian Journal of Animal Sciences 88 (8): 938–943, August 2018.

Agawane S B and Lonkar P S. 2004.Effect of probiotic containing Saccharomyces boulardiion experimental ochratoxicosis in broilers: hematobiochemical studies. Journal of Veterinary Science 5: 359–67.

AOAC. 1995. Official Methods of Analysis. 15th edn. Association of Official Analytical Chemists, Washington, DC.

Baudrimont I, Berbeder A M, Charbi A, Pfohl-Leszkowicz A, Dirheimer G and Creppy E E. 1994. Effect of superoxide dismutase and catalase on the nephrotoxicity induced by subchronical administration of ochratoxinA in rats. Toxicology 89: 101–11.

Belmadani A, Steyn P S, Tramu G, Betbeder A M, Baudrimont I and Creppy E E. 1999. Selective toxicity of ochratoxinA in primary cultures from different brain regions. Archives of Toxicology 73: 108–14.

Denli M, Blandon J C, Guynot M E, Salado S and Perez J F. 2008. Efficacy of a new ochratoxin-binding agent OcraTox to counteract the deleterious effects of ochratoxin A in laying hens. Poultry Science 87: 2266–72.

Devegowda G, Raju M V L N, Afzali N and Swamy H V L N. 1998. Mycotoxin picture worldwide: Novel solutions for their counteraction. Feed Compounder 18: 22–27.

Elaroussi M A, Mohamed F R, El-Barkouky E M, Atta A M, Abdou A M and Hatab M H. 2006. Experimental ochratoxicosis in broiler chickens. Avian Pathology 4: 263–69.

El-Barkouky E M, Mohamed F R, Atta A M, Abu-Taleb A M, ElMenawey M A and Hatab M H. 2010. Effect of Saccharomyces cerevisiae and vitamin C supplementation on broiler performance subjected to ochratoxin A contamination. Egyptian Poultry Science Journal 30: 89–113.

El-Barkouky E M. 2008. The role of yeast in improving the performance of male broiler chicken fed ration contaminated with ochratoxin. Egyptian Journal of Applied Science 23: 13– 24.

El-Barkouky E M and Abu-Taleb A M. 2008. The role of vitamin C in improving the performance of male broiler chickens fed ration contaminated with ochratoxin. Egyptian Journal of Applied Science 23: 1–12.

Garcia A R, Avila E, Rosiles R and Petrone V M. 2003. Evaluation of two mycotoxin binders to reduce toxicity of broiler diets containing ochratoxin A and T–2 toxin contaminated grain. Avian Diseases 47: 691–99.

Hanif N Q, Muhammad G, Siddique M, Khanum A, Ahmed T, Gadahai J A and Kaukab G. 2008. Clinico-pathomorphological, serum biochemical and histological studies in broilers -fed ochratoxin A and a toxin deactivator Mycofix Plus. British Poultry Science 49: 632–42.

Koynarski V, Stoev S, Grozeva N, Mirtcheva T, Daskalo H, Mitev J and Mantle P. 2007. Experimental coccidiosis provoked by Eimeria acervulina in chicks simultaneously fed on ochratoxin A contaminated diet. Research in Veterinary Science 82: 225– 31.

Kubena L F, Harvey R B, Huff W E, Corrier D E, Philips T D and Creger CR. 1988. Influence of ochratoxin A and deoxynivalenol on growing broiler chicks. Poultry Science 67: 253–60.

Kubena L F, Harvey R B, Huff W E, Corrier D E, Philips T D and Rottinghaus G E. 1989. Influence of ochratoxin A and T-2 toxin singly and in combination on broiler chickens. Poultry Science 68: 867–72.

Kubena L F, Philips T D, Creger C R, Witzel D A and Heidelbaugh N D. 1983. Toxicity of ochratoxin A and tannic acid to growing chicks. Poultry Science 62: 1786–92.

Mahesh B K and Devegowda G. 1996. Ability of aflatoxin binders to bind aflatoxin in contaminated poultry feeds. An in vitro study. Proceedings of the 20th World’s Poultry Congress, New Delhi, India. pp 296–303.

Monnet-Tschudi F, Sorg O, Honegger P, Zurich M G, Huggett A C and Schilter B. 1997. Effects of the naturally occurring food Mycotoxin ochratoxin A on brain cells in culture. Neurotoxicology 18: 831–39.

Nahrer K and Kovalsky P. 2014. The biominmycotoxin survey identifying the threats in 2013. Science and Solutions 22: 2– 7.

Omar R F, Hasinoff B B, Mejilla F and Rahimtula A D. 1990. Mechanism of ochratoxin A stimulated lipid peroxidation. Biochemical Pharmacology 40: 1183–91.

Rahimtula A D, Bereziat J C, Bussacchini-Griot V and Bartsch H. 1988. Lipid peroxidation as a possible cause of ochratoxin A toxicity. Biochemical Pharmacology 37: 4469–77.

Sakhare P S, Harne S D, Kalorey D R, Warke S R, Bhandarkar A G and Kurkure N V. 2007. Effect of Toxiroak® polyherbal feed supplement during induced aflatoxicosis, ochratoxicosis and combined mycotoxicoses in broilers. Veterinarski Arhiv 77: 129–46.

Santin E, Paulillo A C, Nakagui L S O, Alessi A C and Maiorka A. 2006. Evaluation of yeast cell wall on the performance of broilers fed diets with or without mycotoxins. Brazilian Journal of Poultry Science 8: 221–22.

Sawale G K, Gosh R C, Ravikanth K, Maini S and Rekhe D S. 2009. Experimental mycotoxicosis in layer induced by ochratoxin A and its amelioration with herbomineral toxin binder toxiroak. International Journal of Poultry Science 8: 798–803.

Shiraishi F, Curtis L M, Truong L, Poss K, Visner G A, Madsen K, Nick H S and Agarwal A. 2000. Heme oxygenase–1 gene ablation or expression modulates cisplatin-induced renal tubular apoptosis. American Journal of Physiology Renal Physiology 278: F726–36.

Singh M, Singh R and Mandal A B. 2016. Use of Saccharomyces cerevisiae to suppress the effects of ochratoxicosis in broiler chickens. Indian Journal of Animal Sciences 86: 790–94.

Singh M. 2015. ‘Influence of dietary Saccharomyces cerevisiae and vitamin E supplementation on ochratotoxicosis in broiler chickens’. M.V.Sc. Thesis, IVRI, Izatnagar, Uttar Pradesh.

Singh R, Mandal A B, Sharma M and Biswas A. 2015. Effect of varying levels of dietary ochratoxin A on the performance of broiler chickens. Indian Journal of Animal Sciences 85: 296– 300.

Singh R, Tyagi P K, Divya and Sharma M. 2013. Ochratoxigenic potential of Aspergillus westerdijkiae NRRL 3174 under laboratory conditions. Indian Journal of Poultry Science 48: 247–49.

Sorrenti V, Giacomo C D, Acquaviva R, Barbagallo I, Bognanno M and Galvano F. 2013. Toxicity of ochratoxin A and its modulation by antioxidants: A review. Toxins (Basel) 5: 1742– 66.

Stanley V G, Ojo R, Woldesenbet S, Hutchinson D H and Kubena L F. 1993.The use of Saccharomyces cerevisiae to suppress the effects of aflatoxicosis in broiler chicks. Poultry Science 72: 1867–72.

Stoev S D, Steanov M, Denev S, Radic B, Domijan A M and Peraica M. 2004. Experimental mycotoxicosis in chickens induced by ochratoxin A and penicillic acid and intervention with natural plant extracts. Veterinary Research Communication 28: 727–46.

Talapatra S K, Ray S C and Sen K C. 1940. Estimation of phosphorus, choline, calcium, magnesium, sodium and potassium in feeding stuffs. Journal of Veterinary Science and Animal Husbandary 10: 243–45.

Varga J and Toth B. 2005. Novel strategies to control mycotoxins in feeds: A review. Acta Veterinari Hungarica 53:189–203.

Verma J, Johri T S, Swain B K and Ameena S. 2004. Effect of graded levels of aflatoxin, ochratoxin and their combinations on the performance and immune response of broilers. British Poultry Science 45: 512–18.

Volkl A and Karlovsky P. 1998. Biological detoxification of fungal toxins and its use in plant breeding and feed and food production. Natural Toxins 7: 1–23.

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Authors:
Ram Singh
Asitbaran Mandal
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