The <scp>l</scp>‐histidine‐mediated enhancement of hydrogen peroxide‐induced cytotoxicity is a general response in cultured mammalian cell lines and is always associated with the formation of DNA double strand breaks

Cantoni, Orazio; Sestili, Piero; Brandi, Giorgio; Cattabeni, F.

doi:10.1016/0014-5793(94)01010-2

Cited by 16 publications

(4 citation statements)

References 13 publications

(4 reference statements)

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“…Our data is in line with other studies showing a pro-oxidant effect of histidine (Oya and Yamamoto, 1988;Tachon and Giacomoni, 1989;Erickson and Hultin, 1992;Cantoni et al, 1994b;Oya-Ohta et al, 2001). In contrast, histidine seems to have protective antioxidant effects at very high concentrations (25 mM and above) (Obata et al, , 2001Obata and Inada, 1999;Obata and Yamanaka, 2000).…”

Section: Discussionsupporting

confidence: 93%

Effects of histidine and imidazolelactic acid on various parameters of the oxidative stress in cerebral cortex of young rats

Tansini

Durigon

Testa

et al. 2004

Intl J of Devlp Neuroscience

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Histidinemia is an inherited metabolic disorder caused by deficiency of histidase activity, which leads to tissue accumulation of histidine and its derivatives. Affected patients usually present with speech delay and mental retardation, although asymptomatic patients have been reported. Considering that the pathophysiology of the neurological dysfunction of histidinemia is not yet understood and since histidine has been considered a pro-oxidant agent, in the present study we investigated the effect of histidine and one of its derivatives, l-beta-imidazolelactic acid, at concentrations ranging from 0.1 to 10 mM, on various parameters of oxidative stress in cerebral cortex of 30-day-old Wistar rats. Chemiluminescence, total radical-trapping antioxidant potential (TRAP), thiobarbituric acid reactive substances (TBA-RS), and the activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were measured in tissue homogenates in the presence of l-histidine or l-beta-imidazolelactic acid. We observed that l-histidine provoked an increase of chemiluminescence and a reduction of TRAP at concentrations of 2.5 mM and higher, while TBA-RS measurement, GSH-Px, CAT and SOD activities were not affected. Furthermore, l-beta-imidazolelactic acid provoked antioxidant effects at high concentrations (5-10 mM) as observed by the reduction of chemiluminescence, although this compound enhanced chemiluminescence at low concentrations (0.5-1 mM). These results suggest that in vitro oxidative stress is elicited by histidine but only at supraphysiological concentrations.

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Section: Discussionsupporting

confidence: 93%

Effects of histidine and imidazolelactic acid on various parameters of the oxidative stress in cerebral cortex of young rats

Tansini

Durigon

Testa

et al. 2004

Intl J of Devlp Neuroscience

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“…Cell survival was determined using a growth inhibition assay described in [13]. After treatments HUVEC were harvested by trypsinization, plated in duplicate at a density of 5 × 10 4 /35 mm dish, and grown for 5 days at 37 • C. Cell proliferation and viability were determined by counting the cells after proper dilution in a hemocytometer; cell death was monitored by counting cells permeated by 0.1% trypan blue.…”

Section: Determination Of Cell Survival and Apoptosismentioning

confidence: 99%

Shiga toxin 1 and ricin inhibit the repair of H2O2-induced DNA single strand breaks in cultured mammalian cells

et al. 2005

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“…It is likely therefore that extracellular amino acids can enter infected cells as easily and, through the supposed transporters of the food vacuole membrane, also enter this compartment. His can also enhance the cytotoxicity of H 2 O 2 (Cantoni et al 1994;Sestili et al 1995) that is vastly produced in infected cells (Atamna and Ginsburg 1993). The inhibition of parasite growth by Cys, His and Trp (albeit at relatively high concentrations) seems therefore to be specific and requires appropriate explanation.…”

Section: Discussionmentioning

confidence: 99%

Killing of intraerythrocytic Plasmodium falciparum by lysosomotropic amino acid esters

et al. 2003

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Esters of amino acids are known to penetrate into cells by simple diffusion. Subsequently, they are hydrolyzed by hydrolases to release the parent amino acid. Due to the abundance of hydrolases in phagolysosomes, amino acids accumulate, there because the rate of influx and hydrolysis exceed the rate of amino acid efflux through specific carriers. The osmotic effect of this accumulation results in the disruption of the organelles. This mechanism has been demonstrated to be responsible for the killing of Leishmania amastigotes by amino acid esters. In this investigation, it is shown that all esters tested, including alcohol esters, N-acetyl esters and the esters of some dipeptides, inhibit the growth of Plasmodium falciparum in culture. Inhibition is timedependent and, in some cases, ring-stage parasites are more sensitive than trophozoites. Similar to the findings with Leishmania, alcohol esters of Glu, Leu, Met, Phe and Trp are more toxic to Plasmodium whereas Ala, Gly, His and Ile are much less noxious. Esters caused the release of acridine orange that selectively accumulates in the phagolysosome-like food vacuole of the parasite, attesting the ostensible destruction of this organelle by osmotic lysis. The toxicity of the N-acetyl esters is probably associated in part to their ability to inhibit cytosolic proteases. Since excess of amino acids can also inhibit proteolysis, the effect of free amino acids on parasite growth was also tested. Of the 19 odd amino acids tested, only three, namely Cys, His and Trp, were found to be toxic to the parasites at millimolar concentrations and the reasons for their possible specific toxicity are discussed.

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The l‐histidine‐mediated enhancement of hydrogen peroxide‐induced cytotoxicity is a general response in cultured mammalian cell lines and is always associated with the formation of DNA double strand breaks

Cited by 16 publications

References 13 publications

Effects of histidine and imidazolelactic acid on various parameters of the oxidative stress in cerebral cortex of young rats

Effects of histidine and imidazolelactic acid on various parameters of the oxidative stress in cerebral cortex of young rats

Shiga toxin 1 and ricin inhibit the repair of H2O2-induced DNA single strand breaks in cultured mammalian cells

Killing of intraerythrocytic Plasmodium falciparum by lysosomotropic amino acid esters

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