Acute Toxicosis of selenium and monensin produced a significant increase in uro- and corpoporphyrin levels. Results also indicated that acute lead toxicosis increased liver porphyrins levels of broiler chickens. This was further aggravated when selenium or monensin were administrated concurrently. This experiment indicated presence of an interaction between lead and selenium or monensin in elevation of porphyrins in the liver tissue of the broiler chickens

Khan, Muhammad Zargham

Szarek, Josef

English

Journals from University of Tartu

Scand, J. Lab. Anun. Sci No 4. 19931V01.20Concurrent exposure to lead, selenium or monensineffects on hepatic porphyrin levelsin broiler chickens during acute toxicosisby JOSQ/‘Szarek and Muhammad Zargham Khan*Department of Forensic Veterinary Medicine and Veterinary Medicine Administration.Faculty of VeLerinary Medicine, University of'Agriculture and Technology,()czapowskiego St. 13, 10-717 Olsztyn, Poland.lnlroduclionMonensin (ionophore) is a antieoeeidialagent which is highly effective against allspecies of eoeeidia in the field together withgrowth promoting properties, It is howeveroeeassionally toxic to animals (Hausmannet all 1991, Khan 1991, Novillu 1992). Ad-ministration of selenium at therapeutic le—vels either prior to or during monensin in—toxication has resulted in a partial protect-ion and amelioration of the toxic effects ofthe drug (Vie?! et a]. 1983, 1985). On theother hand. administration of ”safe“ dosesof monensin to lambs previously intoxicatedwith selenium has exacerbated the toxicityby increased mortality and elevated selen-ium content in various body tissues. Therehave been few reports on the toxic effectsresulting from simultaneous administrationofselenium and monensin. The influence ofthese factors on animal organs in the pre-sence of lead is also very interesting (Madcj01 al. 1988, Szarek & Khan 1992, Zawirxka1981).The increased levels of free erythrocyteproprotoporphyrin (FEP) as well as inhibi-tion of erythrocyte alanine a111i110translerase(ALAD) activity during lead toxieosis hasbeen well documented in birds (Bayer 91 a1.1988, Made} et al. 1988) However. little in—formation is available on avian porphyrinlevels in liver tissue during lead toxieosis.The experiments were performed in the frame-work ofprqieet4.10012011* Present address: N1. Z. Khan, Department ofVeterinary Pathology, Faculty of Veterinary Sci-ence. University of Agriculture, Faisalabad, Paki-Stan.Concurrent administration of lead with sele-nium or other elements or organic com—pounds is known to result in a variable elleelon toxicity (Cerklewski & forbes 1976, Le-vandcr er a1. 1977, Carlson & Nielsen 1985).There is only one report describing thechanges in PE? levels and ALAD activity inerythrocytes of hens during concurrent ad-ministration of lead and selenium (Madej eral. 1988). There are no reports of the effectsof concurrent administration of lead withselenium or monensin on liver porphyrinlevels.The influence that lead selenium and mo—nensin in combination can have on the acti—vity of porphyrin transformation is inter-esting, because it is possible to find thesefactors together naturally in the field (Bayer61 a1. 1988, Beker at al, 1992, Hausmann &Sasse 1991, Mazesic' (’1‘ a1. 1981, Zantopou-[us 61 al. 1992).Materials and methodsBroiler chicks two weeks of age (Astra B)were divided into groups (Table 1) and kepton a diet containing selenium] (15 mg/kg assodium selenitc) (NaZSeOS), selenium plusVitamin E (15 mg Se + 200 mg a~tocophe-rol/kg), monensin (240 mg/kg) as sodiummonensin (Elanco Laboratories, Italy) andlead (1200 mg/kg) as lead acetate (Pb(C2H;0:)2 - 31120) as outlined in Table 1. Thebirds in group 00 were kept on a basal diet,After an adaption period of 12 days on thevarious diets, the birds had lead (2000mg/kg body mass) administrated as a singleoral dose in groups (5L, ESL, ML and CL).231Scund. .1 Lab Amm.Sei.Nn.4.1993.V01.20Table 1. Outline ofthe experiment. Groups No. of birds lst toxic Adaption 2-nd toxic substance,substance in feed period (days) 3 oral doses(mg/kg) (mg/kg body weight)SL 13 selenium (15) 12 lead (2000)ESL 13 selenium (15) lead (2000)plus vitamin E (200)ML 13 monensin (240) 12 lead (2000)LS 13 lead (1200) 12 selenium (8)LM 13 lead (1200) 12 monensin (400)LO 13 lead (1200) 12 noneOL 13 none 12 lead (2000)00 13 none 12 noneBirds in groups LS, LM and LO were orallydosed with selenium (8 mg/kg body mass),monensin (400 mg/kg body mass) and no—thing respectively. Group 00 was kept ascontrol.Outline of the experiment is introduced inTable 1.At 24 hours post intoxication (13.1.) fivebirds were selected at random from eachgroup and sacrificed. Liver was collectedfrom each chicken, weighed and a portionwas preserved in dry ice for porphyrin esti-mation. Porphyrins were extracted from 1i-Ver tissue (Zawirska 1981). Uroporphyrinwas eluted from chromatograms with 5%BC] (Chu & Chu 1955). Qualitative chr0-matographic analysis of prot0« and copro—porphyrin was carried out using the methodsTable 2. Liver porphyrin levels (pg/g) in chickstoxicosis (mean i SD)*.described by Eriksen (1953. 1958). All por—phyrins were assayed quantitatively by spee-trophotometry. Results of porphyrin estima-tions were statistically analysed by the au—alysis of variance and Duncan‘s multiplerange test at probability level 0.05 (Steel &Tome 1960).Experilm‘ma/ resultsDuring acute lead toxicosis the birds kept onbasal food (group 0L) showed increasedlevels of uro-, eopro- and protoporphyrinsin liver. These increases were also found inbirds kept on diets containing selenium(group SL) and selenium plus vitamin E(group ESL).A higher increase was recorded in the birdskept on the diet containing monensin (groupof different groups 24 hours after inducing acute lead Group LeadI Uroporphyrin Coproporphyrin Protoporphyrin l'otal porphyrin(dietary addition) mg .x 10'2 x 10'2 x 10"2 x 10‘?SL(Se) 2000 2.9 : 10c 36 : 0.0b 6.9 : 0.7‘J 13.4 i 1.7bESL(Se+E)7 2000 0 5 _ 0.6ab 4.0 L 1.3b 5.2 : 0.83 9.7 1— 2.7hML(Mon)3 2000 1.8 ,— 0.717c 5.6 : 0.3C 15.2 : 2.3C 22.6 : 3.3COL(~) 2000 1.3 — 0.2"Ih 6.3 i 0.4“ 6.8 : 1.9b 14.4 1 2.5b00 (—) () 0.4 + 0.38 1.9 + 0.98 2.8 t 0.43 5.1 : 1.6a‘ - oral dose given per kg body mass.7- - selenium + Vitamin E.3 - monensm.*232- values with different superscripts appearing in the same column are statistically significant (P < 0.05).Po rphgrins (yg/g)Scand. J. Lab.Anim.Sei.1\'o.4. 1993 . Vol. 20                            30i 22.620— i13.4 % 14.4 -Proto—per ‘11 Igr’ in- 9.7 / 7 _ i10— / / _ I-Copro—. >990 / 5.1 porpl‘tgrirt- (52% xx129%»? 2% g3: g -Uro—D 5‘ _“‘ 2W por'phgrinBrows SL ESL ML BL 00SL — selenium + lead ML — monensin + leadESL— selenium, vita— 0L — leadmin E + lead 00 — noneFig. 1. Liver porphyrine levels in chicks of different groups during acute lead toxieusis at 24 hours postintoxication.ML). Results of the liver porphyrin levelsare shown in the Table 2 and Figure 1.During acute selenium and monensin toxi-cosis in the birds kept on diet containinglead (groups LS and LM, respectively), asignificant increase was recorded in uro- andcoproporphyrin levels, respectively but thetotal porphyrin levels remained insignificant(Table 3).DiscussionAn understanding of porphyrin metabolismin various pathological conditions of theliver is the subject of much research (Beren—son et a]. 1992). It is well-known that leadcauses inhibition of ALAD and ferrochala—tase with subsequent increases in the precur—sors of heme (porphyrins) in tissues of theaffected animals (D055 & Tiepermann 1978).Table 3. Liver porphyrin levels (ttg/g) in Chicks of different groups 24 hours alter acute intoxication withselenium or monensin (mean : SD)*. Group Se/Monensin Uroporphyrin Ceproporphyrin Protoporphyrin Total porphyrin(dietary addition) mgl x 10’2 x 10'2 x 10’2 x 10’2LS (Pb) selenium 1.20 :— 0.0ab 5.54 + 2.5ab 6.46 i 2.9 13.20 L 5.4LM([’b) monensin 2.30 i 1.0h 3.10 : 0.2ab 5.57 i 0.8 10.97 3: 2.0LO(Pb) 0 0.40 i 0.2a 3.03 i 1.1ab 3.10 L 0.1 6.53 i- 1.4OO(—) 0 0.40 i 0.33 1.20 i 0.9a 1.60 + 0.4 3.20 i 1.61 - oral dose given per kg body mass one time only (Se - 8 mg, monensin - 400 mg)."‘ — values with different superscripts appearing in the same column are statistically significant (P < 0.05).233Seantl. .1. 1:111 Amm Sci No 4. 1993 . V01. 20Increased levels of protoporphyrins and de-creased ALAD activity in the erythrocytesof various species of birds have been welldocumented in experimental lead toxieosis(Made/ et al. 1988. Moore 1990, 'l'm‘k er a].1992). Reports however have not mentionedincreased levels of porphyrins in liver duringlead toxieosis as observed in the present ex-periment. A further increase in the liverporphyrin levels in birds kept on diets con—taining monensin and selenium produced anenhancement of lead toxicosis. The role ofselenium and monensin in inducing inere-ased liver porphyrin levels is still not Linder—stood. The morphological and biochemicalincreased liver porphyrin level is vague. Themorphological and biochemical changes re—corded in the birds of different groups ad-ministered lead with selenium or monensin,suggested mitochondrial damage in hepato—cytes with increased levels of lead in theliver (Khan 1991, Szaz'ek & Khan 1992).These changes might have been responsiblefor pronounced disturbances in porphyrinmetabolism of birds during lead toxieosis.The findings in the present experiment de-monstrate that liver porphyrin levels wereelevated in chicks during acute lead toxico-sis. Concurrent administration of seleniumor monensin in the diets further increasedporphyrin levels.Acknowledgemom‘sWe thank Prof. Dr. B. Zawiiska. head 01‘ Chairand Dpt. ot'Pathologieal Anatomy. Medical Aead.in Wroclaw for estimation of hepatic porphyrins.SumnmrtAcute Toxicosis of selenium and monensin pro-duced a significant increase in uro- and corp0~porphyrin levels. Results also indicated that acutelead toxicosis increased liver porphyrins levels ofbroiler chickens. This was further aggravatedwhen selenium or monensin were administratedconcurrently. This experiment indicated presenceof an interaction between lead and selenium ormonensin in elevation of porphyrins in the livertissue ot‘the broiler chickens.SummendingUndersagelser i slagtekyllinger over akutte forgift-ninger af selen 0g monensin viste forhiajet uro- 0g254corpoporfyrin niveau i leveren. Resultaterne fi‘aundersmgelsen indicerede ogsé at akut blyforgift-ning foregede leverporfyrin mveauet i slagtekyllin-ger. Dette blev yderligerc underbygget, nér seleneller monensin blev indgivet samtidig. Dette for-sag indieerer tilstedevzerelsen af en sammenhzengmellem bly 0g selen eller inonensin i foregelsen afporfyrineri leveren hos slagtekyllinger.theem‘rlm K. PL’I/mmwAkuuni seleeni» ja monensiinimyrkytys aiheuttierkitl'a' nousun uroiviin» ja eorpoporlyriinitasoissa.Tulokset viitamat myos sijhen, ettéi akuutti lyijy-myrkytys nosti broilerikanoissa maksan porfyri—initasoja ja tiiméi nousu vielii lisiiéintyi. jos sa-manaikaisesti annettiin seleeniéi j'd. monensiinia.Lyijylléi ja seleenillh’ tai inonensiinilla ll‘ciyttéiiaiolevat vuorovaikutus broilerikanojen maksan por-R({férem'm'Beker D, 7 Romiz‘, H Krsnjmi' & Z Zima: A eon-trihution to the world selenium map. Biol.Trace E1. Res. 1992, 33, 4349.Berenson MM, R Kimurrl, W Summw't: & DBjorkman: Protoporphyrin overload in unre-strained rats: biochemical and histopathologiecharacterisation of a new model 01' protopor-phyrie hepatopathy. 1nt. J. Exp. Path. 1992,73, 665—673,Beyer WN. JW Span”, L Sl'leo & .l(' Fransrm:Lead poisoning in six captive aVJan species.Arch. Environ. Contamin. Toxicol. 1988. 17,121—130.Carlson BL & SW Nilse'n. Influence of dietarycalcium on lead poisoning in mallard ducks(Annas platyrynehos). Am. J. Vet. Res. 1985,46. 276—282.('m‘klpuirlri FL & RM Forbes. Influence of diet-ary selenium on lead toxicity in rats. J. Nutr.1976. 106, 778—783.C/m TC &- EJ (.7111: Paper chromatography ofiron complexes of porphyrins. J. Biol. Chem.1955. 212. 1—7.Doss M (12 RV Tiepm'mann: [Irinary porphyrinprofiles in acute lead poisoning: Relation todifferentiate from acute intermittent porphy-ria. Diagnosis and therapy of porphyria andlead intoxication. Intern. symp. on clinicalbiochemistry 1978, Springer—Verlag, Berlin,Heidelberg. New York.[31‘[A'.3'm1 L: Paper Chromatography of porphyrinpigments. Scand. J. Clin. Lab. Invest. 1953. 5,155—157.Eriksen L: Paper chromatographic separation ofeoproporphyrin isomers I and 111. Seand. .1.C1in.Lab.1nvest. 1958,10487—490.Hammalm R & HHL Screw: MonensinNati-ium—Intoxitation dcr Equiden. Tieréirztl. Umsehau.1991, 46, 127—134.Khan M7. Pathology of b101e1 chicken intoxi-cated with |ead,sele11i11m 01 monensin andtheir combinations. Ph D. thesis 1991 Fa-culty of Vet. Med., Ilniv. Agric. Tech. 01527tyn, Poland.Levander, 0.4, VC Morris (1’1 RJ Ferrari: C0111-parativc effects of selenium and vitamin F, inlead poisoned rats. J. Nutr. 1977, 107, 378—3 .Made) J, G Radzanuwska. S Klimentow5‘k1' & MZar/ca: Zaehowanie sie wybranyeh wskaini~kow hematologieznyeh i bioehcmicznyeh orazzmiany histopatologiezne w narzadaeh kur,ktorym podawano per os Pb, Se oraz Pb + Se.Zesz. Nauk. Akad. Rom, Wroclaw, Wet.1988, 44, 1137127.Matesic D, K K03 &. Amid Slmsek: Koliéinaselena u nekim krmivima i smjesama 2a perads podruejd sr hrvatska. Vet. Arhiv 1981, 51,79—82.Moore MR: An introduction of porphyrins andporphyrias. Molee. Aspects Med. 1990, 11.3—15.Nuvzlla MN: The veterinary importance of thetoxic syndrome induced by ionophores. Vet.Hum. Toxicol. 1992, 34, 66—70.$168! RGD & DJH Torrie: Principles and proce-dures of statistics. McGraw-Hill Book Com-pany Inc. 1960, New York, Toronto. London.Scand. J. Lab. Anim.Se1.Nn.4 . 1993 . Vol 20Szarek / 1&1 M7 Khan Effects of concurrent 2111-ministration of selenium monensin and leadin broiler chicken during subacute toxicosis.1. Pathomorphologieal pattern of liver and he-patie porphyrin levels. Pat. Pol. 1992, 43, 138.Turk DS, DJ Schonfield. M (111/1211 11’. P RmmSensitivity of erythrocyte protoporphyrin asscreening test for lead poisoning New Engl.Joni Med 1992,3215 137—138.View JF van, HE AmAluzz. WE Weird: AH Re-bar 11’: VJ Ferrar15‘./\cute monensin toxieosisin swine; effect of graduated doses 01 moncn-sin and protection of swine by pre-trcatmentwith seleniumivitamin. E. Am. J. vet. Res.1983 44 14601468.Vleet JF van HE Amsmtz & AH Rebcir. Effect ofpre--treatment with selenium-vitamin E onmonensin toxicity in cattle Am J vet. Res.1985, 46, 2221—2228.Zamopoulos N. VArimniou & II Tsoz1kali~Papa-dapoulou: Lead concentrations in plants andanimal tissue. J. Environ. Sei. 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Concurrent exposure to lead, selenium or monensin effects on hepatic porphyrin levels in broiler chickens during acute toxicosis

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Concurrent exposure to lead, selenium or monensin effects on hepatic porphyrin levels in broiler chickens during acute toxicosis

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