Effect of alfatoxins on pig growth and their elimination from the body.

Abstract

EFFECT OF AFLATOXINS ON PIG GROWTH AND THEIR ELIMINATION FROM THE BODY ALEX C. KONDOS Summary l The toxic effect of aflatoxins on pigs, their distribution in -and Results elimination from body tissues were studied in a series of experiments. showed that: 1. the response of growing pigs to diets containing 100, 200 or 400 ppb aflatoxin B was in accordance with the increasing concentration of the toxin 1 and in reverse order to the age of the pigs. While the 100 ppb concentration had no detectable effects on the animals, the 200 ppb depressed appetite, growth The highest or rate and feed conversion efficiency only in the younger pigs. 400 ppb treatment was toxic to pigs throughout the experiment. 2 . Af Latoxins B, and M, were present in the liver, heart, muscle, skeletal muscle and kidnev 24 hours atter treatment but only traces could be detected 48 I hours after administration. .TT Metabolism of aflatoxin B1 was rapid and short term administrations of J. up t o 2 mg B1/pig resulted in only traces of the toxin and its M metabolite 1 being Detectable 24 hours after treatment. T IO INTRODUCTION %-cotoxins and especially aflatoxins, have been recognised for their adverse . effects on animal health and production for many years (Wilson et al. 1967: Wong and Hsish 1976: Swenson et al. 1977; Stoloff 1982; Blaneyet al. 1984: Chauhan et al. 1984: Heathcote 1984: Helferish 1984; Reddy et al. i984; Wilson et al. 7,984). There are well established differences in the susceptibility of various 2.1 LEG L s~ezitts to the effect of aflatoxins (Goldblatt 1969; Patterson 1973; ?.oebuck anti Ijogan 1977) with pigs occupying medium place with regard to sensit i v i t y to these toxins (Jemmali and Murphy 1976; Monegue et al. 1977; Jacobson L e', a l . lw?: Wilson et al. 1984). %!c,orts on the effect of aflatoxins on pig production are rather confusing * three levels a n d ch;! atim o f these investigations was to study the effect of of naturally produced aflatoxins on certain pig production characteristics and t h e mxern cf elimination of aflatoxins from the body tissues of pigs. ^ IF. EXPERIMENTAL (a) Toxicity experiment Large White pigs of mixed sexes anj averagi.ng 22 kg bodv weight were used They were kept in single pens and fed one of in gr!n ps of seven per treatment. fC zr exzerimental diets for 70 days. The four diets had very similar composition (;za se 3, with the main variable being the level of aflatoxins caiculated by I analysis. Their protein content was l8%, lysine 0.9% and were fed to appetite throughout the experiment. There was no evidence of other mycotoxins being preThe source of aflatoxin was a sample of wheat which contained sent in the diets. 505 ppb aflatoxin B I (AFBl) o r 805 p p b o f t o t a l a f l a t o x i n (B1, B2, Gl, G2 Department of Animal Science, Queensland Agricultural College, . Lawe s . L343, Queensland, Australia. and vitamin mixture supplied the following nutrients in air-dry diet: zinc, 55; manganese, 24; copper, 7: iron, 88; selenium, 0.2; vitamins A, 1.2; D, 8.25; E, 0.33; K, 0.66; pantothenic acid, 1 mg: riboflavin, 3.3; pyridoxine, 1.1; biotin. 0.06; choline-&, 1100. (b) Tissue distribution and elimination Large White pigs, weighing approximately 25 kg were individually treated to measuz?: . i. The distribution of aflatoxins in the tissue of liver, heart, kidnev and @teal muscle. Two groups of 6 pigs each were doseddwith 25 or 50 ug Bl/kg Body weight per day for 5 days. Two pigs from each treatment were killed at 3, 24 and 48 hours after the five day aflatoxin administration had been completed. 7 i* The detoxifying efficiencyw of the liver and muscle of pigs subjected to two aflatoxin treatments: (a) Each of two pigs was dosed with a total of 4 mg AFB, in 0.8 mg single daily doses for five days. (b) Another two pigs received the same total dose of 4 mg AFB1 but in two single daily doses of 2 mg each. The pigs were slaughtered 24 hours after the second dose and the liver and muscle were analysed for total AFBl and Ml content. In each experiment, a pig of similar body weight and with the same backgKWld as those used for the aflatoxin observations,but not treated with aflatcxins, were slaughtered and used as controls. (c) Observations In t.k?e growth experiment, growth rate was recorded at 2-weeklv intervals and FCE `da s calculated as being the amount of feed consumed pe; kg weight gain. fn the distribution and elimination experiments, pigs were killed according tc scheduled times and tissue samples weredeep frozen until analysed fcr residual aflatoxins. Results were tested by analysis of variance. III. RESULTS AND DISCUSSION <r The mineral mg kg -I of c9:;;s.t._ 0.7; I+f-ac in, 16; '12, 0.019; (a) Toxicity Experiment The toxic effects of the three aflatoxin treatments were assessed over the whole experimental period using as criteria the growth rate, feed conversion efficiency, feed intake and any other signs shown by the.aflatoxin treated pigs iz relation to the 0 level control group. Results are presented in Table 2 and Figure !. The effect of the aflatoxin treatments on the growth of pigs started becoming apparent as from the end of the first two experimental weeks when the 200 2nd LOO ppb treatments appeared to exert a significantly depressing (P(o.05) . ef feet on growth. As the experiment progressed, the differences in weight gain between the control and the 400 ppb treatment increased (P(O.01) but by the end Of t:?e tenth week. onlv the 400 ppb treatment remained significantly (P<O.Ol) be low the other three kroups. From the mean progressive weight gain in each treatment group (Table 2b), it can be deduced that the most severe growth depression was caused by the two The higher highest aflatoxin treatments with the youngest pigs suffering most. degree of susceptibility of younger pigs to aflatoxins has also been reported by Wogan (1968). By the end of the experiment, pigs on the 400 ppb treatment had gained about 33% less weight than the control. There is conflicting information regarding the lower concentration at which aflatoxins start causing measurable toxic effects on pigs, a rather complex area which can be influenced by a variety of biological and environmental The present results showed that while a 200 ppm concentration of AFBl factors. or 319 ppb of total aflatoxin (B + B2 + G1 + G ) was toxic to younger pigs, it 2 1 had no effect on older pigs. On the contrary, 400 ppb AFBl or 631 ppb total, affected all ages. Although Kelly and Booth (1971) reported that 230 ppm B1 did not cause any toxicity to growing pigs and Monegue et al. (1977) could not detect any appreciable growth depression in pigs fed diets containing 300-500 ppm, on the other hand, Krogh et al. (1973) found that similar levels to those used in our experiments reduced appetite and depressed pig growth. In most of the published data, aflatoxin toxicity has been associated with the presence of the B 1 aflatoxin only, while the other three aflatoxins G G > are usually present with Bl and have also been found to be toxic. (3 7? 1' Cokequent ? y they can contribute to the overall toxicity but to a lesser extent in reiation to AFB . The feed intike results (Table 3), in their totality, reflect the growth The 200 ppb treatment was the lowest level at which an rate pa ttern of p i g s . appreciab le reduction in feed intake could be detected. Tabie 3 . Mean feed consumption in kg/pig per treatment and feed conversion efficiency (in brackets) 3ecause of the possible effect of aflatoxins o n the metabolic functions of the animal, Feed Conversion Efficiency was used to assess whether the growth depression was due to reduced appetite only or to both appetite and me tabolic functions. Results give a good indication of the differences in FCE between treatments and especially the consistently inferior mean values amongst the pigs Although this is only indicative of the possible effects in the 400 ppb groupon metabolic functions, assessment of the biological significance of such disturbances in the ability of pigs to efficiently utilize nutrients in the presence of aflatoxins would need a more detailed biochemical study. It is known that the litter, which isthe central organ for biochemical transformations, is the target organ for damage by aflatoxins (Polan et al. 1974: Rodricks and Stolloff 1977; Campbell 1977; Stolloff, 1980; Miller e t al.1984: Helferish, 1986: Gill et a1.1984; . Butler, 1984). Lijinsky et al.- (1970), found that aflatoxin B1 or one of its metabolites might bind to nucleic acids and proteins resulting in the biological inactivation of these compounds. Similar results, where DNA and RNA had been implicated, have also been reported by Swenson et al. (1973.), Gurtoo and Bejba (1974), Ashoor and Chu (1975) and Croy et al. (1978). Their findings showed that aflatoxins can interfere with protein synthesis in the animal, thus reducing the efficiency of protein utilization and consequently growth rate. According to Patterson (1977), the high hepatotoxic activity of aflatoxin B1 could be due to an activated hemiacetal form of the toxin which in turn binds to and inactivates certain metabolic liver systems. From the present results, it appears that the magnitude of toxicity caused by 100-200 ppb AFBl was low and this could be due to the high,aflatoxin metabolising capabilities of the pig up to that level of aflatoxinadministration (see next experiment). As soon as the level of the toxin was increased to 400 ppb, the tolerance level was exceeded and more severesigns of toxicity become evident. (b) Distribution and elimination of aflatoxins from body tissues ~~~~~ \ LOW level AFBl over five d a y s (i1 bummary of the results on the' distribution of AFBl in and its elimination from bodv tissues of pigs is presented in Table 4. Tagle 4= Distribution and elimination of aflatoxin B1 from pig tissues following a two-level treatment The results indicate.that, f o l l o w i n g administration of AFb at the 1 w.. c r &CL&-d uf 25 or SO ug/kg bodv weight, very small amounts remained in the muscle of pigs siauehtereci 24 hours after treatment and only traces at 48 hours. The'&-droxvlated Ml metabolite of AFBl was found to be present at very low leveis onlv in the liver and kidney tissue of pigs slaughtered 3 hours afte; remov2 1 o&he toxin from the feed. No measurable amount of MI was found in pigs slaughtered 24 hours after the aflatoxin contaminated feed was withdrawn. The rapid metabolism and excretion of AFBl from the body may be one of the factors contri buting to the appreciable degree of tolerance of the pig to the toxic effects of aflatoxins. No aflatoxin was detected in the control pigs. The practical importance of the results is that if an aflatoxin contaminated feed had been fed to pigs, the carcass should be considered safe for human consumption about 48 hours after such feed was removed. (ii) High level AFBl over 2 or 5 davs Results from these experiments are presented in Table 5. Table 5. Level of B, and M, in the liver and muscle of Pigs (ug/kg) Despite the low residual level of B1 and M in the liver and muscle tissue 1 24 hours after end of treatment, there is a distinct difference between the two treatments in the absolute concentration of residual aflatoxins in each tisstze. 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