[Effects of alpha-tocopherol on partial functions of the ischemic kidney].

The experiments on 45 rats and 20 rabbits were made to investigate antiischemic efficacy of alpha-tocopherol in respect of various partial functions of the kidneys compared to its antioxidant activity. It is demonstrated that administration of alpha-tocopherol prior to 30-min heat ischemia arrests activation of membrane lipid peroxidation (LPO) in the tissue of ischemic kidney both in rabbits and rats. Rabbit filtration renal function 1 hour after circulation recovery improved insignificantly, 24 hours after the recovery no difference with the control was registered, while secretory and reabsorption functions of the renal tubules under conditions of pretreatment with alpha-tocopherol significantly improved both in rabbits and rats both 1 hour and 24 hours after ischemia. Estimation of Ca-ATP activity of a microsomal fraction of the cortical substance of the ischemic kidneys has detected alpha-tocopherol induced suppression of LPO in sub-cellular membrane and high activity of this enzyme. Mechanisms of different protective action of alpha-tocopherol on renal glomeruli and tubules are discussed.

[The membrane phospholipid peroxidation and Ca-dependent ATPase activity of the microsomal fractions isolated from rat renal tissue in thermal ischemia with and without alpha-tocopherol protection]. / Perekisnoe okislenie membrannykh fosfolipidov i Ca-zavisimaia ATFaznaia aktivnost' mikrosomnykh fraktsii, vydelennykh iz pochechnoi tkani krys pri teplovoi ishemii bez protektsii i s protektsiei al'fa-tokoferolom.

The author studied the effects of 30-min heat ischemia of rat kidneys on the level of malonic dialdehyde (MDA) and Ca-dependent ATPase activity of microsomal fraction isolated from the cortical substance in the presence and absence of antibiotic alameticine and ortovandate in the incubation medium and protective action on Ca-ATPase activity of rat pretreatment with alpha-tocopherol (TP). It has been demonstrated that thermal ischemia induces inhibition of Ca-ATPase activity of microsomes resistant to vanadate. Administration of TP reduced MDA level, enhanced Ca-ATPase microsomal activity in the presence of alameticine against inhibition of enzymic activity in the absence of alameticine. This indicates a rise in the true enzyme activity under decreasing membrane permeability in conditions of diminishing activity of lipid peroxidation in response to TP effects.

[Lipid peroxidation and Ca-dependent ATPase activity in the microsomal fraction of renal tissue in patients with nephrolithiasis and chronic pyelonephritis]. / Perekisnoe okislenie lipidov i Ca-zavisimaia ATFaznaia aktivnost' mikrosomnoi fraktsii pochechnoi tkani bol'nykh nefrolitiazom i khronicheskim pielonefritom.

The author has estimated levels of malonic dialdehyde (MDA) indicative of activity of membrane phospholipid peroxidation activity, basal and true (in incubation in the culture containing glomeruloform antibiotic alameticin) Ca-ATPase activity in microsomal fraction isolated from cortical tissue of functioning kidneys obtained intraoperatively from 26 patients. 12 samples of cortical tissue obtained from uninvolved parts of the kidneys affected with carcinoma served as control. 14 samples were obtained from the tissue of functioning kidneys affected with nephrolithiasis and active chronic pyelonephritis. The investigations show elevated MDA levels, enhanced basal in reduced true Ca-ATPase activity of microsomes from the kidneys of patients with nephrolithiasis and active chronic pyelonephritis compared to control. It is suggested that high basal against low true Ca-ATPase activity of renal microsomes may be explained by increased permeability of renal membranes for Ca2+ under activation of lipid peroxidation in active chronic pyelonephritis and nephrolithiasis.

[Lipid peroxidation in the kidney tissue of patients with nephrolithiasis and chronic pyelonephritis]. / Perekisnoe okislenie lipidov v pochechnoi tkani bol'nykh nefrolitiazom i khronicheskim pielonefritom.

Lipid peroxidation (LPO) activity has been analyzed in homogenates and microsomes of cortical samples obtained intraoperatively from the kidneys of 33 patients. Of them, 21 patients had mild, moderate or severe pyelonephritis or nephrolithiasis. Unaffected cortical tissue from renal carcinoma patients was used as control. LPO activity was judged by basal level of malonic dialdehyde (MDA) and MDA growth in the homogenate and microsomes following initiation of ascorbate-dependent LPO. Activation of LPO was registered in patients with moderate disease with active inflammation. They also exhibited greater MDA basal levels and rapid MDA increase in response to in vitro initiation of ascorbate-dependent LPO simultaneously with attenuation of endogenous antioxidant defense. In severe pyelonephritis and nephrolithiasis with drastic deficiency of renal function LPO activity was low and nonresponsive to stimulation either by ascorbate or Fe+2. This is probably due to lack of the substrate after massive death of renal cells. Enhancement of LPO activity in patients with pyelonephritis or nephrolithiasis against functioning kidneys may appear responsible for destruction of renal tissue.

[The importance of studies of calcium reabsorption and of the capacity of the blood plasma to inhibit Ca-ATPase activity for the diagnosis of the activity of the inflammatory process and for the prognosis of tubular function in patients with chronic pyelonephritis]. / Znachenie issledovanii reabsorbtsii kal'tsiia i sposobnosti plazmy krovi ingibirovat' Ca-ATFaznuiu aktivnost' dlia diagnostiki aktivnosti vospalitel'nogo protsessa i prognozivovaniia sostoianiia kanal'tsev u bol'nykh khronicheskim pielonefritom.

The contribution of pyelonephritis activity to calcium reabsorption defects was investigated in 176 patients with chronic pyelonephritis (CP) aged 18-54 with normal tubular filtration and calcium serum concentrations under calcium reabsorption above 98%. 86 of these patients had CP complicated by nonocclusive pelvic stones. Ca-excretory capacity of the kidneys was evaluated with estimation of the excreted calcium by activity phases considering individual deviations or without them. Measurements were also made of CP activity and severity by the inhibition of Ca-ATPase activity of the microsomes isolated from rat intact kidneys. The findings indicate that in active CP calcium-reabsorption impairments related to the inflammation are combined with the preexisting ones, the changes being more pronounced with growing activity of the inflammation, irrespective of the presence of nephrolithiasis. The relationship established between the shifts in excreted calcium induced by inflammation and plasma ability of CP patients to inhibit Ca-ATPase activity of rat renal microsomes in single tests in the same patients allows assessment of calcium reabsorption changes due to CP activity in patients when analysing their blood inhibitory effect on the test enzyme system. Simultaneous one-stage determination in CP patients of their blood inhibition in response to the test enzyme system and excreted calcium helps prognosticate calcium reabsorption expected in remission.

[The suppression of the Ca ATpase activity of rat kidney microsomes under the action of blood plasma as an index of the severity of the status of pyelonephritis patients]. / Ugnetenie Ca-ATFaznoi aktivnosti mikrosom pochek krys pod deistviem plazmy krovi kak pokazatel' tiazhesti sostoianiia bol'nykh pielonefritom.

Whether blood plasma from 63 pyelonephritis patients can inhibit Ca-ATPase activity when compared to known toxicity marker (middle-sized molecule number) was studied. This was done to assess diagnostic potentialities of the test based on the ability of plasma from pyelonephritis patients to inhibit the test enzymatic system, i. e. Ca-ATPase activity of the microsome fraction from renal cortex in intact rats. The inhibition of Ca-ATPase activity by the plasma is shown to correlate with inflammation activity and the patients condition. In pyodestructive acute pyelonephritis this inhibition reached 60.6 +/- 3.86%, in acute serous pyelonephritis 36.02 +/- 1.54%. It follows, that the above parameter is more informative than the number of middle-sized molecules and can be introduced as one of the criteria of the patients' condition and for choice of treatment.

[Lipid peroxidation in a kidney tissue homogenate from rats under heat-induced ischemia with and without glucocorticoid protection]. / Perekisnoe okislenie lipidov v gomogenate pochechnoi tkani krys pri teplovoi ishemii bez i s protektsiei gliukokortikoidami.

Lipid peroxidation (LPO) was investigated in cortical layer homogenates from 56 rat kidneys, intact or exposed to a 30-minute heat ischemia performed without any protection or after a preliminary administration of prednisolone alone or in combination with methypred. Prednisolone was administered i.m. in a dose of 30 mg/kg 2 hrs before and the same dosage of methypred a day before the onset of the experiment. Homogenates were studied both for the initial levels of malonic dialdehyde (MDA) and for the MDA formation in the presence of LPO which was activated in the phosphate buffer by pH 6.8 ascorbate (5.10(-4) M) 5, 10, 15, 20, 25 and 30 minutes after the incubation. The results obtained demonstrated that versus the intact kidneys, in the kidneys exposed to a 30-minute treatment with heat ischemia there were increased levels of initial MDA in the renal tissue, a dramatic increment of its formation during the incubation of homogenate with ascorbate. Shifts in the kinetic curves in homogenates from ischemic kidneys were noted as well. A more dramatic rise (versus intact kidneys) in the MDA formation levels in the presence of LPO observed at the initial stage of the incubation was suggestive of an exhaustive effect of heat ischemia on the system of endogenous antioxidants. The dramatic increment of MDA levels was recorded during a 30-minute incubation. Administration of prednisolone alone or in combination with methypred resulted in a significant inhibition of LPO in ischemic renal tissue.(ABSTRACT TRUNCATED AT 250 WORDS)