Concentrations and lipid peroxidation in tissues and toxicity of para-aminobenzoic acid fed to rats in drinking water

1996 ◽  
Vol 7 (7) ◽  
pp. 408-413 ◽  
Author(s):  
Te-Yang Chang ◽  
Miao-Lin Hu
2021 ◽  
Vol 100 (4) ◽  
pp. 406-410
Author(s):  
Olha Ye. Fedoriv ◽  
Alexandra Ye. Kopach ◽  
Nataliia A. Melnyk

Introduction. Given the significant prevalence of lead in the environment, research in this area has significant social and economic importance. Lead compounds are characterized by high toxicity and increased ability to cumulate in ecosystems, humans, and animals. Lead enters the human body with food, drinking water, atmospheric air, and smoking. Lead causes pathological changes in the nervous system, blood-forming organs, kidneys, etc. Materials and methods. The experiments were carried out on four groups of white female rats, each included seven animals, weighing 150-200 g. The first group of animals was a control. The second group consumed dechlorinated water from the city water supply, followed by lead acetate. The animals from the third and fourth groups drank the same water with sodium stearate and potassium stearate content in a dose of 1/250 LD50. After the 40th-day of the use of these waters, the animals were orally administered lead acetate at a dose of 7 mg/kg. The levels of lipid peroxidation biomarkers were studied by studying the content of diene conjugates (DC) and malondialdehyde (MDA) in blood serum, liver, and kidney homogenates. Results. The administration of 1/2 acetate LD50 to lead in experimental rats drinking water with stearates was accompanied by a significant increase in the DCs concentration and (MDA) in animals. Higher concentrations of LPO products were observed in the group of animals that consumed water from potassium stearate. Conclusions. 1. With the oral administration of lead acetate against the background of drinking water containing stearates at a dose of 1/250 LD50, an increase in lipid peroxidation indices was noted compared with the control group. 2. Higher concentrations of LPO products were observed in the group of animals consuming water from potassium stearate.


2009 ◽  
Vol 297 (1) ◽  
pp. H86-H92 ◽  
Author(s):  
Burton M. Altura ◽  
Nilank C. Shah ◽  
Xian-Cheng Jiang ◽  
Zhiqiang Li ◽  
José Luis Perez-Albela ◽  
...  

The present study tested the hypothesis that short-term dietary deficiency of magnesium (Mg) (21 days) in rats would 1) result in decreased serum(s) [the present study tested the levels of Mg, sphingomyelin (SM), and phosphatidylcholine (PC)]; 2) promote DNA fragmentation, lipid peroxidation (LP), and activation of caspase-3 in cardiac (ventricular and atrial) and vascular(aortic) muscle; and 3) low levels of Mg2+ added to drinking water would either prevent or greatly ameliorate these manifestations. The data indicate that short-term Mg deficiency (10% normal dietary intake) resulted in profound reductions in serum-ionized Mg and total Mg with an elevation in serum-ionized calcium (Ca2+), significant lowering of serum SM and serum PC, with concomitant LP, DNA fragmentation, and activation of caspase-3 in ventricular (right and left chambers), atrial (right and left chambers) and abdominal aortic smooth muscle. The greater the reduction in serum-ionized Mg, the greater the effects on DNA fragmentation, LP, and caspase-3 activity. The intake of water-borne Mg2+ at all levels greatly attenuated or inhibited the reductions in serum SM and serum PC, activation of LP, DNA fragmentation, and the activation of caspase-3; even very low levels of Mg2+ in drinking water (i.e., 15 parts·million−1·day−1) were cardio- and vascular protective. In addition, we demonstrate that short-term dietary deficiency of Mg probably results in a downregulation of SM synthase and a decreased synthesis of PC.


Author(s):  
O. V. Lototska

Introduction One of the reasons for the lack of quality drinking water is the poor quality of natural water, which is constantly polluted by waste water from industrial and municipal enterprises, surface runoff from the fields and territories of settlements with which it enters a large amount of toxic substances. Among them, surface-active substances such as potassium and sodium stearate are not the last.The aim of the study to determine the specifics of lipid peroxidation and the state of the antioxidant protection under the influence of potassium and sodium stearates on the body of the experimental rats when they enter with drinking water.Research Methods. White rats were divided into 7 groups, which consumed water with stearates in quantities equal to the maximum non-active dose of the substance (MND), 1/2 MND and 1/4 MND for 25 days. The content of TBC-active lipid peroxidation products, diene conjugates and the activity of superoxide dismutase and catalase in liver homogenate were determined.Results and Discussion. In the homogenate of the liver of animals of all groups, there was a significant increase in the level of diene conjugates and TBK-active products in proportion to the concentration of the substance. It was also found that in animals that consumed water with different concentrations of potassium stearate, inhibition of antioxidant enzymes was observed. Consumption of water with different concentrations of sodium stearate caused the activation of these enzymes.Conclusions. Prolonged use by test animals of aqueous solution with  concentrations of potassium and sodium stearate in MND and 1/2 MND negatively affects the state of hepatocyte cell membranes due to the activation of the lipid peroxidation processes, namely TBK-active products and diene conjugates, the amount of which depended on the concentration of stearates in drinking water. The use of drinking water by test animals with maintenance of potassium and sodium stearates at various doses caused changes in the content of antioxidant enzymes: water with potassium stearate inhibits the activity of these indicators, and causes sodium activation with sodium stearate.


2006 ◽  
Vol 22 (9) ◽  
pp. 375-380 ◽  
Author(s):  
Meral Oncu ◽  
Kanat Gulle ◽  
Erdal Karaoz ◽  
Fatih Gultekin ◽  
Sureyya Karaoz ◽  
...  

This experiment was designed to investigate the lipid peroxidation and histological effects of chronic fluorosis on first and second generation rat lung tissues. Sixteen, virgin, female Wistar rats were mated with eight males (2:1) for approximately 12 h to obtain first-generation rats. Pregnant rats were divided into two experimental groups (control and fluoride supplemented). The pregnant rats in the fluoride-supplemented group were exposed to 30 mg/L sodium fluoride (NaF) in commercial drinking water containing 0.07 mg/L NaF throughout the gestation and lactation periods. After the lactation period, young animals (first generation; F1) were exposed to the same amount of NaF in drinking water for four months. At the end of the four-month experimental period, nine randomly-chosen male rats (F1) were sacrificed and lung tissues were removed for histopathological and enzymatic lipid peroxidation examination. The second generation rats were obtained from the remaining rats by the same method. They were also treated similarly. At the end of the four-month experimental period, nine randomly-chosen male rats (F2) were sacrificed, and the lungs were removed for histological and lipid peroxidation examination. The rats in the control groups underwent the same procedure without NaF supplementation. It was found that the plasma fluoride and the lung TBARS levels of fluoride supplemented F1 and F2 rats were higher than controls. There were marked histological changes in the lung tissues of fluoride supplemented F1 and F2 rats, as follows: in F1 rats; loss of alveolar architecture, emphysematous areas, descuamation of alveolar epithelium and alveolar congestion were observed. There were thickened interalveolar septae and congestion of alveolar septal vessels. Intraparenchymal thick-walled vessels were also observed. There were markedly perivascular and intraparenchymal focal mononuclear cell infiltrations. In F2 rats, in addition to these changes, there were lipid cell hyperplasia and increased connective tissue mass in the parenchymal areas. It is concluded that chronic fluorosis causes a marked destruction in lung tissues of F1 and F2 rats by causing lipid peroxidation. Toxicology and Industrial Health 2006; 22: 375-380.


2010 ◽  
pp. n/a-n/a ◽  
Author(s):  
Agnieszka Ścibior ◽  
Halina Zaporowska ◽  
Irmina Niedźwiecka

2019 ◽  
Vol 2 (3) ◽  
pp. 15-18 ◽  
Author(s):  
S. О. Slobodian ◽  
B. V. Gutyj ◽  
K. Y. Leskiv

Lipid peroxidation is a form of tissues respiration. This process is characteristic of normal tissues and occurs, as a rule, after the construction of lipid membrane structures, their updates and during the biosynthesis of many hormones. However, free radical oxidation can be activated in an unfavorable environmental situation, since in our case it happened under the action of Cadmium and Lead. The purpose of the work was to investigate the Cadmium and Lead effects on the lipid peroxidation processes intensity in rats. The experiments were carried out on 200 – 220 g male “Wistar” rats, from which 4 groups of animals were formed: 1) control group – animals were administered drinking water through a metal probe in bulk, which is equivalent to the volume of aqueous salt solution Cd2+ і Pb2+; 2) experimental group 1 – animals were administered 0.029 % an aqueous solution of cadmium chloride in a dose 4.0 mg/kg; 3) experimental group 2 – animals were administered 16.6 % aqueous lead acetate solution at a dose 200 mg/kg; 4) experimental group 3 – animals were administered 16.6 % aqueous lead acetate solution at a dose 100 mg/kg and 0.029 % an aqueous solution of cadmium chloride in a dose 2.0 mg/kg. Throughout the experiment, rats were kept in a balanced diet containing all the necessary components, the animals were given drinking water without restrictions from 0.2 liter glass bowls. Based on our research, we detected activation of lipid peroxidation (LPO) products in the blood of rats under lead-cadmium loading, as indicated by the growth of intermediate and final products in comparison with the group of intact animals. Probable level increase of LPO products was observed from the first day of the experiment. For the 7th day of the experiment, the level of diene conjugates in the blood of the third experimental group increased by 88.9 %, and the level of Thiobarbituric acid reactive substances (TBARS) increased by 31.8 %. At 14 and 21 days of the experiment, the level of of LPO products in the rats blood under the lead-cadmium load was the highest. These changes in the LPO products level indicate an increase in the intensity of radical formation processes. Peroxide oxidation forms, at almost all stages of its course, a number of products that result from the interaction of free radicals with each other and with biological macromolecules.


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