Abstract:Spontaneous and stimulated lipid peroxidation (LPO) after vanadate and magnesium treatment was studied in kidney supernatants obtained from outbred 5-month-old, albino male Wistar rats. The 2-month-old animals daily received: group I (control), deionized water to drink; group II, water solution of sodium metavanadate, NaVO(3) (SMV, 0.125 mg V ml(-1)); group III, water solution of magnesium sulfate, MgSO(4) (MS, 0.06 mg Mg ml(-1)); and group IV, water solution of SMV-MS at the same concentrations as in groups I… Show more
“…All details concerning the methodology of determination of LPO and the preparation of kidney homogenates and supernatants for the renal MDA k and TAS k measurements had already been provided [2, 3]. The results of both the OS markers mentioned are expressed as % of control and illustrated in Figure 4(a).…”
Section: Methodsmentioning
confidence: 99%
“…Its prooxidant action has been demonstrated in in vivo and in vitro conditions [2–7]. It has been shown that the free radical process-lipid peroxidation (LPO), which is a biochemical biomarker of cellular dysfunction and an index of cytotoxicity [8], is enhanced by V in the kidney [3, 8]. It has also been suggested that LPO may be predictive of renal dysfunction [8].…”
The alterations in the levels/activities of selected biomarkers for detecting kidney toxicity and in the levels of some oxidative stress (OS) markers and elements were studied in male rats to evaluate biochemically the degree of kidney damage, investigate the role of OS in the mechanism of functional renal disorders, reveal potential biomarkers of renal function, and assess the renal mineral changes in the conditions of a 12-week sodium metavanadate (SMV, 0.125 mg V/mL) exposure. The results showed that OS is involved in the mechanism underlying the development of SMV-induced functional renal disturbances. They also suggest that the urinary cystatin C (CysCu) and kidney injury molecule-1 (KIM-1u) could be the most appropriate to evaluate renal function at the conditions of SMV intoxication when the fluid intake, excreted urinary volume (EUV), body weight (BW), and the urinary creatinine excretion (Creu) decreased. The use of such tests as the urinary lactate dehydrogenase, alkaline phosphatase, γ-glutamyltranspeptidase, and N-acetyl-β-D-glucosaminidase (LDHu, ALPu, GGTPu, and NAGu) seems not to be valid given their reduced activities. The use of only traditional biomarkers of renal function in these conditions may, in turn, be insufficient because their alterations are greatly influenced by the changes in the fluid intake and/or BW.
“…All details concerning the methodology of determination of LPO and the preparation of kidney homogenates and supernatants for the renal MDA k and TAS k measurements had already been provided [2, 3]. The results of both the OS markers mentioned are expressed as % of control and illustrated in Figure 4(a).…”
Section: Methodsmentioning
confidence: 99%
“…Its prooxidant action has been demonstrated in in vivo and in vitro conditions [2–7]. It has been shown that the free radical process-lipid peroxidation (LPO), which is a biochemical biomarker of cellular dysfunction and an index of cytotoxicity [8], is enhanced by V in the kidney [3, 8]. It has also been suggested that LPO may be predictive of renal dysfunction [8].…”
The alterations in the levels/activities of selected biomarkers for detecting kidney toxicity and in the levels of some oxidative stress (OS) markers and elements were studied in male rats to evaluate biochemically the degree of kidney damage, investigate the role of OS in the mechanism of functional renal disorders, reveal potential biomarkers of renal function, and assess the renal mineral changes in the conditions of a 12-week sodium metavanadate (SMV, 0.125 mg V/mL) exposure. The results showed that OS is involved in the mechanism underlying the development of SMV-induced functional renal disturbances. They also suggest that the urinary cystatin C (CysCu) and kidney injury molecule-1 (KIM-1u) could be the most appropriate to evaluate renal function at the conditions of SMV intoxication when the fluid intake, excreted urinary volume (EUV), body weight (BW), and the urinary creatinine excretion (Creu) decreased. The use of such tests as the urinary lactate dehydrogenase, alkaline phosphatase, γ-glutamyltranspeptidase, and N-acetyl-β-D-glucosaminidase (LDHu, ALPu, GGTPu, and NAGu) seems not to be valid given their reduced activities. The use of only traditional biomarkers of renal function in these conditions may, in turn, be insufficient because their alterations are greatly influenced by the changes in the fluid intake and/or BW.
“…The daily intake of water and the solutions of SMV, MS, and SMV-MS were measured with a measuring cylinder and the water and fluid intake was expressed as mL/rat/24 h. In turn, the daily intake of V and Mg in the SMV- or/and MS-administered animals was estimated on the basis of the 24 h consumption of the SMV, MS, and SMV-MS solutions and expressed as mg/kg b.wt./24 h. However, the food intake was calculated on the basis of the 24 h consumption of food by the rats from all the groups (the remainder of food together with additional spillage was weighed and subtracted from the whole food that the rats received to eat) and expressed as g/rat/24 h. The V and Mg concentrations in drinking water were selected on the basis of our previous experiments conducted in a rat model [11, 12, 36] and studies of other researchers [37, 38]. The concentration of V was chosen to reveal its prooxidant potential, which was meant to be attenuated by the administration of this element in combination with Mg.…”
Section: Methodsmentioning
confidence: 99%
“…However, in some conditions Mg may stimulate LPO causing OS. Its ability to elevate LPO has been revealed by us [11, 12] and by some other investigators [27]. …”
Section: Introductionmentioning
confidence: 91%
“…In certain conditions, it may enhance the generation of oxygen-derived reactive species and stimulate LPO [10]. Its prooxidant properties have been revealed in in vivo and in vitro conditions both by us [11, 12] and by some other researchers [10, 13–21]. On the other hand, antioxidant action of V [22], its insulin-like effects [23], and anticarcinogenic activity [24–26] have also been reported.…”
The protective effect of magnesium as magnesium sulfate (MS) on sodium-metavanadate- (SMV-) induced lipid peroxidation (LPO) under in vivo and in vitro conditions was studied. The 18-week SMV intoxication (Group II, 0.125 Vend/mL) enhanced spontaneous malondialdehyde (MDA) generation in rat liver, compared with the control (Group I) and MS-supplemented animals (Group III, 0.06 Mgend/mL). Coadministration of SMV with MS (Group IV, SMV-MS) caused a return of the MDA level to the control value range. The effect seems to result from the Mgend-independent action and its antagonistic interaction with Vend. The in vitro treatment of liver supernatants (LS) obtained from all the tested animals groups with selected exogenous concentrations of Feexg or Vexg exhibited enhanced MDA production, compared with spontaneously formed MDA. It also showed Mgexg-stimulating effect on LPO (LS I, Group I) and revealed that the changes in the MDA generation in LS IV (Group IV) might have resulted from the synergistic interactions of Vend with Feexg and Vexg and from the antagonistic interactions of Mgend with Feexg and Vexg. The findings allow a suggestion that adequate Mg intake for a specific period in the conditions of SMV exposure may prevent V-induced LPO in the liver.
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