Effect of Hydrazine on Protein Content of Various Tissues in the Rat

Banks, William L.; Stein, Eduardo R.

doi:10.3181/00379727-120-30425

Cited by 5 publications

(3 citation statements)

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“…The decrease in the levels of AST in the liver is in agreement with previous reports and indicates the direct hepatotoxic effect of Hz on the metabolism of carbohydrates and proteins in the liver tissue (Stein et al, 1971). The disruption of protein metabolism is further evident by an increase in the levels of protein in both the serum and liver tissue of Hz-treated rats (Table 1) in agreement with previous reports (Amenta and Johnston, 1963;Banks and Stein, 1965;Korty and Coe, 1967).…”

Section: Discussionsupporting

confidence: 93%

Protective Effect of Picroliv Against Hydrazine-Induced Hyperlipidemia and Hepatic Steatosis in Rats

Vivekanandan

Gobianand

Priya

et al. 2007

Drug and Chemical Toxicology

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The protective effect of picroliv (PIC) obtained from Picrorhiza kurroa (family: Scrophulariaceae) against hydrazine (Hz)-induced hyperlipidemia was evaluated in rats. Hz administration (50 mg/kg, i.p.) caused an increase in triglyceride (TG), cholesterol (CHO), free fatty acids (FFA), and total lipids (TL) in both the plasma and liver tissue of rats accompanied by a fall in phospholipids (PL) in the liver tissue 24 h after its administration, indicating its hyperlipidemic property. The above abnormality was prevented by simultaneous treatment of PIC (50 mg/kg, p.o.) with Hz. Hz treatment also caused an increase in the mobility of TG and TL from adipose tissue, and these results indicate that Hz administration could cause hepatic steatosis by nonhepatocellular factors (such as mobilization of depot fats). This effect was also prevented by simultaneous treatment of PIC with Hz. PIC-alone treatment, however, did not produce any change in the status of all the lipid parameters evaluated in plasma, liver, and adipose tissues. These results indicate that increased mobilization of depot fats from adipose tissue may contribute to the development of hepatic steatosis in addition to decreased lipoprotein secretion, increased hepatic TG biosynthesis, and increased hepatic uptake of FFA. These have been reported as the mechanism responsible for the development of Hz-induced hepatic steatosis. PIC prevents Hz-induced hyperlipidemia, hepatic steatosis, and mobilization of lipids from depot fats, but the mechanism behind the protective effect of PIC remains to be elucidated.

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Section: Discussionsupporting

confidence: 93%

Protective Effect of Picroliv Against Hydrazine-Induced Hyperlipidemia and Hepatic Steatosis in Rats

Vivekanandan

Gobianand

Priya

et al. 2007

Drug and Chemical Toxicology

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“…The larger ratio of k in / k out in the liver for gliclazide, glipizide, glibenclamide and glimepiride is presumably indicative of a combination of greater permeability of the liver and more binding in the liver than the pancreas. There is a higher tissue protein concentration in the liver, 112.8 mg protein g −1 liver,34 than in the pancreas, 83.1 mg protein g −1 protein (unpublished result from our laboratory) and the associated greater number of nonspecific binding sites. Consistent with our findings, glibenclamide has been shown to have a greater partitioning into the liver than into the pancreas after intravenous injection 35…”

Section: Discussionmentioning

confidence: 81%

Sulphonylurea physicochemical-pharmacokinetic relationships in the pancreas and liver

Fanning

Anissimov

Roberts

2009

Journal of Pharmaceutical Sciences

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This study examined the physicochemical-pharmacokinetic relationships for the sulphonylureas in the perfused rat pancreas and liver. Multiple indicator dilution studies were conducted with bolus injections of tolbutamide, chlorpropamide, gliclazide, glipizide, glibenclamide and glimepiride, and a reference marker albumin, in the perfused pancreas and liver. Individual solute pharmacokinetics were analysed using nonparametric moment analysis and nonlinear regression assuming a physiologically based pharmacokinetic model. All solutes had similar shaped outflow concentration-time profiles in both the pancreas and liver, but varied in extraction. Negligible drug extraction was evident in the pancreas. Hepatic extraction ranged from 0.03 (tolbutamide) to 0.52 (glibenclamide) and could be related to solute lipophilicity and perfusate protein binding. The sulphonylurea mean transit times in both the pancreas and liver varied four- and ninefold respectively and were related to the lipophilicity and perfusate protein binding of the drug. The permeability surface area product of sulphonylureas from the perfusate into the organs were greater in the liver and were mainly determined by lipophilicity (pancreas, r2 = 0.89; liver, r2 = 0.80). The distribution of the sulphonylureas in both the perfused pancreas and perfused liver was dependent on their lipophilicity and perfusate protein binding.

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“…This inhibition could be reversed by the addition of pyridoxal phosphate to the reaction mixture (Killam and Bain, 1957;McCormick and Snell, 1961). Banks and Stein (1965) have also demonstrated that liver RNA and liver protein are concomitantly elevated in hydrazine-treated rats, thus the authors suggest an in vivo stimulation of liver protein synthesis by hydrazine. Simonsen and Roberts (1967) have published data on the influence of hydrazine on the distribution of free amino acids in mouse liver.…”

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confidence: 91%