Search

Current findings aimed to find out camel milk's effects on lipid metabolism, expression of the genes for antioxidant enzymes and paraoxonase-1 (PON-1) activity in rats fed diet-containing cholesterol 1%. Therefore, 30 rats were divided into three groups (10 rats per each). Rats of the first group, which acted as a control group, fed a basic diet. Rats of the second group fed a basal diet that included 1% cholesterol however, rats of the third group fed cholesterol 1% accompanied by oral administration of camel's milk (100mL/24h/cage/5 rats) as the only source of water for them. Diet of cholesterol 1% induced significant increase in serum total cholesterol, triacylglycerol (TAG), low-density lipoprotein cholesterol (LDL-c), alanine aminotransferase (ALT), aspartate aminotransferase (AST) activities whereas lower serum PON-1 activity was observed when compared to control. Diet of cholesterol 1% induced significant increase in hepatic Thiobarbituric acid reactive substance (TBARS) however, compared to the control, a significant decrease in the activity and gene expression of antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPX), glutathione-S transferase (GST), and reduced glutathione (GSH) were detected. These detrimental effects were ameliorated into accepted range in camel milk treated group. Fatty degeneration and fatty cysts in liver tissues were detected in rats fed cholesterol diet but the affected liver showed acceptable degree of recovery in camel milk treated group. Conclusively, camel milk was potential for the treatment of hyperlipidemia and hypercholesterolemia in rats.

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. PEKTIN VPLIVA NA IZBOLJŠANJE HEMATOLOŠKIH IN BIOKEMIJSKIH PARAMETROV, HISTOPATOLOGIJE, BIOLOŠKIH OZNAČEVALCEV OKSIDATIVNEGA STRESA, CITOKINOV TER IZRAŽANJE GENA ZA HEPCIDIN PRI S SVINCEM POVZROČENI TOKSIČNOSTI PRI PODGANAH 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