• Sabry M. El-Bahr Department of Biomedical Sciences, College of Veterinary Medicine, King Faisal University, Al-Ahsa, 31982, Saudi Arabia; Department of Biochemistry, Faculty of Veterinary Medicine, Alexandria University, Alexandria, 21523, Egypt, Corresponding author, E-mail:
  • Saad Al-Sultan Department of Biomedical Sciences, College of Veterinary Medicine, King Faisal University, Al-Ahsa, 31982; Department of Public Health, College of Veterinary Medicine, King Faisal University, Al-Ahsa, 31982, Saudi Arabia
  • Ahlam F. Hamouda Department of Forensic Medicine and Toxicology, Teaching Hospital, Faculty of Veterinary Medicine, Benha University, Benha, 13736, Egypt
  • Shimaa A. E. Atwa Department of Biochemistry, Faculty of Veterinary Medicine, Benha University, Benha, 13736, Egypt
  • Seham Y. Abo-Kora Department of Pharmacology, Faculty of Veterinary Medicine, Benha University, Benha, 13736, Egypt
  • Aziza A. Amin Department of Histopathology, Faculty of Veterinary Medicine, Benha University, Benha, 13736, Egypt
  • Saad Shousha Department of Biomedical Sciences, College of Veterinary Medicine, King Faisal University, Al-Ahsa, 31982, Saudi Arabia; Department of Physiology, Faculty of Veterinary Medicine, Benha University, Benha, 3736, Egypt
  • Sameer Alhojaily Department of Biomedical Sciences, College of Veterinary Medicine, King Faisal University, Al-Ahsa, 31982, Saudi Arabia
  • Aymmen Alnehas Department of Clinical Sciences, College of Veterinary Medicine, King Faisal University, Al-Ahsa, 31982, Saudi Arabia
  • Rabab R. Elzogby Department of Pharmacology, Faculty of Veterinary Medicine, NewVally University, Egypt



lead acetate, toxicity, pectin, hepcidin, oxidative stress biomarkers, histopathology


Publications concerning the protective effect of pectin against lead induced toxicity in rats are not available. In order to study such effect, 40 male rats were divided into 3 groups. The first group was contained 10 rats that kept as control group. The second group was contained 10 rats that received pectin at dose of 100 mg/kg BW during experimental period (8 weeks). The third group was contained 20 rats that received 400mg/kg BW of lead acetate daily for 4 weeks then divided into two subgroups (3A and 3B). Subgroup 3A contained 10 rats that still receive lead acetate in the same dosage whereas, subgroup B co-treated with lead acetate and pectin daily for another 4 weeks. Blood samples were collected after 2, 4 and 8 weeks from the start of the experiment. Liver, kidney and bone marrows were collected only at the end of the experiment. Lead acetate induced anemia only after 4 weeks of administration as reflected on decreased values of Hb, PCV, MCV, MCH and MCHC. These indices remained at lower levels in lead acetate treated groups until the end of the experiment. Concentrations of serum ferritin, iron, total antioxidant capacity (TAC) and reduced glutathione (GSH) and the expression of hepatic hepcidin gene were decreased significantly in lead acetate intoxicated rats compared to control. Activities of ALT and AST and concentrations of urea, creatinine, Nitric oxide (NO), TNF-α, IL-6, total iron binding capacity (TIBC) and lead were increased significantly in lead acetate intoxicated group compared to control. Hepatic degeneration and hemorrhage, renal lytic necrosis and apoptosis of myeloid cells were most prominent changes in lead intoxicated rats. Lead acetated related changes were improved by co-treatment with pectin however; normal control val- ues have not been achieved. Conclusively, pectin is recommended to protect against lead acetate toxicity in rats.


Izvleček: Objav o zaščitnem učinku pektina pred toksičnostjo svinca pri podganah ni na voljo. Da bi proučili ta učinek, smo 40 samcev podgan razdelili v 3 skupine. V prvi, kontrolni skupini je bilo 10 podgan. V drugi skupini je bilo 10 podgan, ki so v poskus- nem obdobju (8 tednov) prejemale pektin v odmerku 100 mg/kg telesne teže. V tretji skupini je bilo 20 podgan, ki so 4 tedne dnev- no prejemale svinčev acetat v odmerku 400 mg/kg telesne teže. Tretja skupina je bila nato razdeljena v dve podskupini (3A in 3B). V podskupini 3A je bilo 10 podgan, ki so še naprej 4 tedne prejemale svinčev acetat v enakem odmerku, v podskupini 3B pa je 10 podgan prejemalo svinčev acetat in pektin. Vzorci krvi so bili odvzeti po 2, 4 in 8 tednih od začetka poskusa. Ob koncu poskusa so bili odvzeti še jetra, ledvice in kostni mozeg. Svinčev acetat je povzročil anemijo šele po štirih tednih, kar se je kazalo v zmanj- šanih vrednostih Hb, PCV, MCV, MCH in MCHC. V skupini podgan, ki so prejemale svinčev acetat, so te vrednosti do konca po- skusa ostale nizke. Koncentracije serumskega feritina, železa, skupne antioksidativne kapacitete (TAC), reduciranega glutationa (GSH) in izražanje jetrnega gena za hepcidin so se pri podganah, ki so prejemale svinčev acetat, znatno zmanjšale v primerjavi s kontrolo. Aktivnosti ALT in AST ter koncentracije sečnine, kreatinina, dušikovega oksida (NO), TNF-α, IL-6, skupne kapacitete vezave železa (TIBC) in svinca so se v skupini, ki je prejemala svinčev acetat, znatno povečale v primerjavi s kontrolno skupino. Najvidnejše spremembe pri podganah, ki so prejemale svinec, so bile jetrna degeneracija in krvavitve, ledvična nekroza in apop- toza mieloidnih celic. Spremembe, povezane s svinčevim acetatom, so se izboljšale s sočasnim zdravljenjem s pektinom, vendar normalne kontrolne vrednosti niso bile dosežene. Zaključili smo, da je pektin priporočljiv za zaščito pred toksičnostjo svinčevega acetata pri podganah.

Ključne besede: svinčev acetat, toksičnost, pektin, hepcidin, biološki označevalci oksidativnega stresa, histopatologija


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