Determination of tissue susceptibility to oxidative stress by enhanced luminescence technique

Venditti, Paola; Leo, T. De; Meo, S. Di

doi:10.1016/s0076-6879(99)00131-7

Cited by 27 publications

(26 citation statements)

References 11 publications

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“…However, we obtained some information on the effectiveness of the antioxidant system by a method able to evaluate tissue sensitivity to oxidative processes (Venditti et al, 1999). In this method the extent of oxidative changes occurring in conditions leading to increased in vivo ROS production is obtained by measuring the levels of light emission resulting from in vitro exposure to H 2 O 2 of tissue homogenates.…”

Section: Discussionmentioning

confidence: 99%

“…It has been shown that the values of parameters a and b are dependent on the concentration of substances able to induce and inhibit, respectively, the H 2 O 2 -promoted luminescence reaction (Venditti et al, 1999). It has also been shown that substances able to induce the luminescence reaction include Fe 2+ complexes, such as the haemoproteins, which promote the conversion of H 2 O 2 into reactive · OH radicals via the Fenton reaction (Halliwell and Gutteridge, 1990), whereas substances inhibiting the luminescence reaction include antioxidants able to prevent the formation of or interact with · OH radicals.…”

Section: Discussionmentioning

confidence: 99%

“…GSH concentration was measured in homogenates as described by Griffith (Griffith, 1980). The response to oxidative challenge was determined as previously described (Venditti et al, 1999). In brief, samples of 10% (w/v) homogenates were obtained by diluting the 20% homogenates with equal volumes of 0.2% Lubrol in 15 mmol l -1 Tris, pH 8.5.…”

Section: Analytical Proceduresmentioning

confidence: 99%

“…The relationship between light emission (E) and homogenate concentration (C) was described by the equation E=aC/exp(bC), where a and b are two constants (Venditti et al, 1999). A careful examination of this function shows that b is the inverse of the homogenate concentration at the emission maximum (E max ), which, in turn, is determined by a and b values (E max =a/eb).…”

Section: Response To Oxidative Challengementioning

confidence: 99%

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T3 and the thyroid hormone β-receptor agonist GC-1 differentially affect metabolic capacity and oxidative damage in rat tissues

Venditti

Chiellini

Bari

et al. 2009

Journal of Experimental Biology

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SUMMARYWe compared the changes in tissue aerobic metabolism and oxidative damage elicited by hypothyroid rat treatment with T 3 and its analog GC-1. Aerobic capacities, evaluated by cytochrome oxidase activities, were increased more by T 3 than by GC-1. Furthermore, the response of the tissues to T 3 was similar, whereas the response to GC-1 was high in liver, low in muscle and scarce in heart. Both treatments induced increases in ADP-stimulated O 2 consumption, which were consistent with those in aerobic capacities. However, unlike T 3 , GC-1 differentially affected pyruvate/malate-and succinate-supported respiration, suggesting that respiratory chain components do not respond as a unit to GC-1 stimulation. According to the positive relationship between electron carrier levels and rates of mitochondrial generation of oxidative species, the most extensive damage to lipids and proteins was found in T 3 -treated rats. Examination of antioxidant enzyme activities and scavenger levels did not clarify whether oxidative damage extent also depended on different antioxidant system effectiveness. Conversely, the analysis of parameters determining tissue susceptibility to oxidants showed that pro-oxidant capacity was lower in GC-1-than in T 3 -treated rats, while antioxidant capacity was similar in treatment groups. Interestingly, both agonists decreased serum cholesterol levels, but only GC-1 restored euthyroid values of heart rate and indices of tissue oxidative damage, indicating that GC-1 is able to lower cholesterolemia, bypassing detrimental effects of T 3 .

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Analytical Proceduresmentioning

confidence: 99%

Section: Response To Oxidative Challengementioning

confidence: 99%

See 2 more Smart Citations

T3 and the thyroid hormone β-receptor agonist GC-1 differentially affect metabolic capacity and oxidative damage in rat tissues

Venditti

Chiellini

Bari

et al. 2009

Journal of Experimental Biology

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“…Response to oxidative challenge was determined as previously described (Venditti et al, 1999). Briefly, samples of 10% (w:v) homogenates were obtained by diluting the 20% homogenates with equal volumes of 0.2% Lubrol in 15·mmol·l -1 Tris, pH·8.5.…”

Section: Susceptibility To Oxidative Challengementioning

confidence: 99%

Differential effects of experimental and cold-induced hyperthyroidism on factors inducing rat liver oxidative damage

Venditti¹,

Pamplona

Ayala

et al. 2006

Journal of Experimental Biology

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SUMMARY Thyroid hormone-induced increase in metabolic rates is often associated with increased oxidative stress. The aim of the present study was to investigate the contribution of iodothyronines to liver oxidative stress in the functional hyperthyroidism elicited by cold, using as models cold-exposed and 3,5,3′-triiodothyronine (T3)- or thyroxine(T4)-treated rats. The hyperthyroid state was always associated with increases in both oxidative capacity and oxidative damage of the tissue. The most extensive damage to lipids and proteins was found in T3-treated and cold-exposed rats, respectively. Increase in oxygen reactive species released by mitochondria and microsomes was found to contribute to tissue oxidative damage, whereas the determination of single antioxidants did not provide information about the possible contribution of a reduced effectiveness of the antioxidant defence system. Indeed, liver oxidative damage in hyperthyroid rats was scarcely related to levels of the liposoluble antioxidants and activities of antioxidant enzymes. Conversely,other biochemical changes, such as the degree of fatty acid unsaturation and hemoprotein content, appeared to predispose hepatic tissue to oxidative damage associated with oxidative challenge elicited by hyperthyroid state. As a whole, our results confirm the idea that T3 plays a key role in metabolic changes and oxidative damage found in cold liver. However,only data concerning changes in glutathione peroxidase activity and mitochondrial protein content favour the idea that dissimilarities in effects of cold exposure and T3 treatment could depend on differences in serum levels of T4.

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Effect of Exercise Duration on Characteristics of Mitochondrial Population from Rat Liver

Venditti

Masullo

Meo

1999

Archives of Biochemistry and Biophysics

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Determination of tissue susceptibility to oxidative stress by enhanced luminescence technique

Cited by 27 publications

References 11 publications

T3 and the thyroid hormone β-receptor agonist GC-1 differentially affect metabolic capacity and oxidative damage in rat tissues

T3 and the thyroid hormone β-receptor agonist GC-1 differentially affect metabolic capacity and oxidative damage in rat tissues

Differential effects of experimental and cold-induced hyperthyroidism on factors inducing rat liver oxidative damage

Effect of Exercise Duration on Characteristics of Mitochondrial Population from Rat Liver

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