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Changes in blood pressure and plasma catecholamines caused by tyramine and cold exposure.

Tyramine may be used to stimulate release of endogenous norepinephrine. We have compared the increases in blood pressure and plasma catecholamines in normal volunteers during (a) tyramine infusions, and (b) the more physiological sympathetic stimulus of cold exposure. In a second study, the cardiac component of the pressor effect of tyramine was assessed by measuring systolic time intervals, and by infusing tyramine in beta-blocked subjects. Tyramine, 15.0 micrograms/kg/min for 30 min, elevated systolic BP from 122 +/- 11 to 149 +/- 4 mm Hg, without increasing diastolic BP or heart rate. Plasma norepinephrine rose from 0.547 +/- 0.184 to 0.836 +/- 0.096 ng/ml; plasma epinephrine was unchanged. Thirty-min exposure to 4 degrees C elevated both systolic BP (from 105 +/- 8 to 116 +/- 9 mm Hg) and diastolic BP (from 72 +/- 4 to 81 +/- 6 mm Hg). This was associated with a greater rise in plasma norepinephrine, from 0.357 +/- 0.131 to 1.143 +/- 0.393 ng/ml; plasma epinephrine was again unchanged. A single oral dose of propranolol 160 mg caused approximately a two-fold right shift in the systolic BP dose response to tyramine, and blocked the tyramine-induced shortening of the presystolic ejection period. Tyramine appears to exert its pressor effect mainly by stimulation of cardiac beta-receptors. This may account for the relatively small rise in plasma norepinephrine (relative to cold exposure) since the heart does not contribute a high proportion of circulating norepinephrine.

Adult↗

PubMed2004

Tyramine receptor (SER-2) isoforms are involved in the regulation of pharyngeal pumping and foraging behavior in Caenorhabditis elegans.

Octopamine regulates essential processes in nematodes; however, little is known about the physiological role of its precursor, tyramine. In the present study, we have characterized alternatively spliced Caenorhabditis elegans tyramine receptor isoforms (SER-2 and SER-2A) that differ by 23 amino acids within the mid-region of the third intracellular loop. Membranes prepared from cells expressing either SER-2 or SER-2A bind [3H]lysergic acid diethylamide (LSD) in the low nanomolar range and exhibit highest affinity for tyramine. Similarly, both isoforms exhibit nearly identical Ki values for a number of antagonists. In contrast, SER-2A exhibits a significantly lower affinity than SER-2 for other physiologically relevant biogenic amines, including octopamine. Pertussis toxin treatment reduces affinity for both tyramine and octopamine, especially for octopamine in membranes from cells expressing SER-2, suggesting that the conformation of the mid-region of the third intracellular loop is dictated by G-protein interactions and is responsible for the differential tyramine/octopamine affinities of the two isoforms. Tyramine reduces forskolin-stimulated cAMP levels in HEK293 cells expressing either isoform with nearly identical IC50 values. Tyramine, but not octopamine, also elevates Ca2+ levels in cells expressing SER-2 and to a lesser extent SER-2A. Most importantly, ser-2 null mutants (pk1357) fail to suppress head movements while reversing in response to nose-touch, suggesting a role for SER-2 in the regulation of foraging behavior, and fail to respond to tyramine in assays measuring serotonin-dependent pharyngeal pumping. These are the first reported functions for SER-2. These results suggest that C. elegans contains tyramine receptors, that individual SER-2 isoforms may differ significantly in their sensitivity to other physiologically relevant biogenic amines, such as octopamine (OA), and that tyraminergic signaling may be important in the regulation of key processes in nematodes.

Adrenergic Uptake Inhibitors↗

PubMed1985

Predominant sensitivity to tyramine in the isolated intermediate auricular artery of the dog.

Using a steel cannula inserting method, the action of tyramine on segments of similar size from isolated intermediate auricular and mesenteric arteries of the dog was investigated. In intermediate auricular arteries, intra-luminally administered tyramine caused strong vasoconstriction, i.e. the threshold dose for inducing constriction was about 0.03 to 0.1 micrograms and at a dose of 3 micrograms the tyramine-induced increase in perfusion pressure was usually more than 200 mm Hg. On the other hand, in mesenteric arteries, tyramine caused only a small increase in perfusion pressure, i.e. the threshold dose was about 1 to 3 micrograms and the maximum level of the increase in perfusion pressure was only 15 to 30 mm Hg even at the large dose of 100 micrograms. The tyramine-induced constriction was blocked by pretreatment with imipramine. Potassium chloride-induced constriction was not inhibited by imipramine in doses which markedly suppressed tyramine-induced responses. Imipramine failed to potentiate the effects of noradrenaline but rather suppressed them in a dose-related manner in both arteries. In intermediate auricular arteries from reserpine-pretreated dogs, the effect of tyramine was attenuated whilst that of noradrenaline was significantly enhanced. Both arterial preparations responded well to periarterial electrical nerve stimulation but at lower stimulus frequencies, intermediate auricular arteries were more responsive than mesenteric arteries. It is suggested that the intermediate auricular artery of the dog has predominant sensitivity to intraluminally administered tyramine which may be related to the role of this vessel in the regulation of cutaneous blood flow.

Animals↗

PubMed1970

Restoration of tyramine responses by bretylium, BW392C60, bethanidine and monoamine oxidase inhibitors in reserpine-treated rats.

1. Bretylium, BW392C60, bethanidine, nialamide and pheniprazine, but not guanethidine or ouabain, were all capable of restoring the cardiovascular response to tyramine in reserpine pretreated rats anaesthetized with sodium pentobarbitone.2. In parallel with their recorded in vitro activity as monoamine oxidase inhibitors, BW392C60 was found to be more potent at restoring the response to tyramine than bretylium or bethanidine.3. The restored responses to tyramine were completely blocked by desmethyl-imipramine or by a combination of phentolamine and propranolol.4. The effect of bretylium on the tyramine response was not influenced by bilateral adrenal demedullation, urethane anaesthesia, the dose or duration of the reserpine pretreatment and was not dependent upon the frequency of the tyramine injections.5. Bretylium, BW392C60 or bethanidine did not alter the pressor response to intravenous noradrenaline.6. Nialamide-induced restorations of the responses to tyramine were not further enhanced by the administration of bretylium, BW392C60 or bethanidine.7. In pithed reserpine-treated rats the ability of bretylium and BW392C60 to restore the response to tyramine was reduced.8. It is concluded that all the drugs which reversed the reserpine-induced subsensitivity to tyramine were acting as monoamine oxidase inhibitors, thus allowing the intra-neuronal accumulation of endogenously formed catecholamines. The presence of nerve impulses in the adrenergic fibres of reserpinized rats appears to be an important factor in mediating this effect.

Adrenalectomy↗

PubMed1982

Relationship between tyramine potentiation and selective inhibition of monoamine oxidase types A and B in the rat vas deferens.

1 The degree of selective monoamine oxidase (MAO) inhibition produced by (-)-deprenyl, clorgyline, LY51641 and tranylcypromine was examined in relation to modification of tyramine and noradrenaline contractile responses of the rat isolated vas deferens. 2 All inhibitors possessed reversible alpha-adrenoceptor blocking activity, determined against noradrenaline on the denervated vas deferens. For LY51641 and tranylcypromine, antagonism was competitive, with pA2 values of 6.17 and 5.16. 3 Clorgyline, LY51641 and (-)-deprenyl (10(-5) M) inhibited the tyramine response while present in the organ bath: LY51641, which was the most potent as an alpha-adrenoceptor blocker, produced this effect at 10(-6) M. Responses to tyramine and noradrenaline were potentiated on wishing out the inhibitors, but noradrenaline potentiation was seen only when tyramine had been present in the system. 4 Tranylcypromine (10(-6) M) potentiated responses to noradrenaline and tyramine while present in the organ bath. 5 Potentiation of tyramine responses by clorgyline and LY51641 occurred at 91% and 64% inhibition of MAO type A respectively, although full potentiation of the tyramine response was elicited only when substantial inhibition of both enzyme types occurred. Selective inhibition of MAO type B by 67% (with deprenyl) was not associated with tyramine potentiation.

Adrenergic alpha-Antagonists↗

PubMed1995

Characterization of the vasorelaxant activity of tyramine and other phenylethylamines in rat aorta.

We recently reported that tyramine caused concentration-dependent relaxation of rat aorta, which was endothelium independent and was not exerted via alpha 1-adrenoceptors (AR), alpha 2AR, beta 1AR, beta 2AR, or receptors for 5-hydroxytryptamine, histamine, and adenosine. The present studies were done on endothelium-denuded strips to determine structure-vasorelaxant activity after blockade of beta AR by propranolol plus irreversible blockade of alpha 1AR with benextramine. Vasorelaxation under these conditions was limited to noncatecholamines, and their vasorelaxant potencies were methoxyphenamine > tyramine > p-hydroxyephedrine > L-amphetamine > L-ephedrine > phenylethylamine > synephrine > methoxamine > octopamine. beta 3AR agonists (BRL 37344 and CGP 12177A) did not produce vasorelaxation, although tyramine could compete for cyanopindolol binding to murine L cells expressing human beta 2AR or beta 3AR. There was no significant specific binding of [3H]tyramine to aortic membrane preparations after the inhibition of monamine oxidase. Yohimbine, which has a high affinity for Drosophila tyramine receptors, also caused dose-dependent vasorelaxation like tyramine. It is concluded that tyramine and several other phenylethylamines produce relaxation of rat aorta, which does not involve any of the known adrenoceptors but may be exerted via novel tyramine receptors.

Animals↗

PubMed2005

Modulation of tyramine signaling by osmolality in an insect secretory epithelium.

The control of water balance in multicellular organisms depends on absorptive and secretory processes across epithelia. This study concerns the effects of osmolality on the function of the Malpighian tubules (MTs), a major component of the insect excretory system. Previous work has shown that the biogenic amine tyramine increases transepithelial chloride conductance and urine secretion in Drosophila MTs. This study demonstrates that the response of MTs to tyramine, as measured by the depolarization of the transepithelial potential (TEP), is modulated by the osmolality of the surrounding medium. An increase in osmolality caused decreased tyramine sensitivity, whereas a decrease in osmolality resulted in increased tyramine sensitivity; changes in osmolality of +/-20% resulted in a nearly 10-fold modulation of the response to 10 nM tyramine. The activity of another diuretic agent, leucokinin, was similarly sensitive to osmolality, suggesting that the modulation occurs downstream of the tyramine receptor. In response to continuous tyramine signaling, as likely occurs in vivo, the TEP oscillates, and an increase in osmolality lengthened the period of these oscillations. Increased osmolality also caused a decrease in the rate of urine production; this decrease was attenuated by the tyraminergic antagonist yohimbine. A model is proposed in which this modulation of tyramine signaling enhances the conservation of body water during dehydration stress. The modulation of ligand signaling is a novel effect of osmolality and may be a widespread mechanism through which epithelia respond to changes in their environment.

Animals↗

PubMed1984

Mechanism of tyramine-induced migraine: similarity with dopamine and interactions with disulfiram and propranolol in migraine patients.

In a double-blind crossover study, 8 patients with classical migraine received disulfiram (400 mg/day) for 6 days, alternating with matched placebo tablets at 2 weekly intervals. Intravenous dopamine and tyramine pressor tests were performed on the 3rd and 6th days of each phase, respectively. 50-75% of patients experienced migraine attacks within 24 h of a test. There was no difference in the incidence of attacks between dopamine and tyramine injections. The number of migraine-free days was more during the placebo week than during disulfiram treatment (p less than 0.05). The post-tyramine migraine index correlated directly with the amount of tyramine administered during the dose-response test (r = 0.66), but no such relationship was found with dopamine. In a further study, post-tyramine migraine was observed in only 1 of 5 patients treated with propranolol (80 mg/day) for 4 weeks. Neither disulfiram nor propranolol influenced the tyramine pressor sensitivity. It is concluded that increased adrenergic activity is responsible for more frequent attacks during disulfiram medication. A similar mechanism probably is responsible for post-dopamine/tyramine migraine in susceptible subjects. It is unlikely that tyramine plays any specific role, except via its effect on the adrenergic system, in the pathogenesis of migraine attacks. However, the tyramine challenge test can be useful in the evaluation of a putative antimigranous activity of a new drug.

Adult↗

PubMed1983

Basic and clinical reevaluation of tyramine and histamine tests for the investigation of adrenomedullary sympathetic functions.

In vitro and in vivo studies using histamine and tyramine tests were carried out to investigate adrenomedullary sympathetic functions. Administration of 10(-3) M tyramine enhanced catecholamine release from both the perifused swine adrenal medulla and human pheochromocytoma tissue, whereas histamine did not show this effect. Tyramine also induced release of catecholamine from the isolated catecholamine granules in vitro, but histamine did not. The tyramine or histamine test was performed in vivo on groups of 16 subjects, respectively, consisting of healthy adults and hypertensive patients. In all cases, a rise in blood pressure was observed after loading with either tyramine or histamine. On the other hand, when urinary catecholamine output was examined during the first 2 h after loading, a significant increase was not observed in 4/16 after tyramine administration, and in 6/16 after histamine loading. Thus, using an in vitro system, we showed a difference between tyramine and histamine in the mode of direct action on adrenal medulla. We also conclude that urinary catecholamine output is of less significance than the blood pressure response as an index of tyramine or histamine test.

Adrenal Gland Neoplasms↗

PubMed1986

The effects of amiflamine, a reversible MAO-A inhibitor, on the first pass metabolism of tyramine in dog intestine.

The effects of amiflamine on tyramine deamination were studied using isolated loops of intestine in anesthetized dogs. In the pretreatment experiment, dogs were dosed with amiflamine (3.5 mg/kg/day) once daily for 3 days, with the study being carried out 3 hr after the final dose. [14C] Tyramine (50 mg and 50 microCi) in 10 ml of normal saline was introduced into the isolated loops of gut, and tyramine and p-hydroxyphenylacetic acid in the venous blood were separated by HPLC and measured by scintillation spectrometry. In the untreated dogs, approximately 15% of the tyramine passed through the gut wall unchanged. When tyramine and amiflamine (0.06 to 3.5 mg/kg) were administered simultaneously to the gut loop, about 27 to 65% of the tyramine passed through the gut wall unchanged. On the contrary, after pretreatment with amiflamine for 3 days, percentage of tyramine passing through the gut wall was not increased in comparison with the control. These results suggest that pretreatment with amiflamine does not produce drug concentrations in the lining cells of the gut sufficient to effectively inhibit the deamination of oral tyramine, which is administered at least 3 hr after the final dose of amiflamine.

Animals↗

PubMed1996

Paracetamol (acetominophen) sulphoconjugation in man: no correlation with tyramine sulphoconjugation.

There is considerable evidence that subjects vulnerable to endogenous depression excrete less tyramine sulphate after an oral dose of free tyramine than controls (the tyramine test). In this study, 26 psychiatric inpatients, exhibiting a wide range of responses to the test, and 10 normal controls were challenged with oral doses of paracetamol and tyramine on two separate occasions. Urinary output of paracetamol sulphate and paracetamol glucuronide in all subjects was monitored but there were no significant correlations with tyramine sulphate output. Thus, the output of these metabolites appears to be under complex control, and paracetamol cannot be substituted for tyramine in the "tyramine test". The basic deficit responsible for low values in the tyramine test is unlikely to stem from sulphate depletion or a generalised disturbance of the sulphation system, and remains obscure.

Acetaminophen↗

PubMed1988

Interaction of moclobemide, a new reversible monoamine oxidase inhibitor with oral tyramine.

In a double-blind placebo-controlled cross-over study in 8 healthy volunteers possible interactions between moclobemide and tyramine were studied. Eight volunteers received either moclobemide or placebo for a period of 6 days and received tyramine on day 5 and day 6 of each treatment period. Moclobemide was given in a daily dose of 450 mg to be taken in three divided doses at the end of the meals. Tyramine was administered in the form of an artificially tyramine enriched cheese (camembert) together with a meal at noon. The total tyramine doses administered were 50 mg on day 5 and 100 mg on day 6 of each treatment period. Comparisons of blood pressure and heart rate changes after tyramine ingestion between moclobemide and placebo conditions did not indicate any relevant moclobemide-tyramine interaction. It is concluded that tyramine in quantities of up to 100 mg does not lead to clinically relevant blood pressure reactions in moclobemide-treated subjects, if moclobemide is taken at the end of the meal.

Administration, Oral↗

PubMed1984

Blockade of ganglionic afterdischarges by tyramine may be mediated by endogenous catecholamines.

Tyramine reduced the compound postganglionic action potential from preganglionic stimulation of the golden hamster isolated stellate ganglion at 0.2 Hz. This action of tyramine was only slightly reduced by phentolamine (10(-5)M), an alpha adrenoceptor antagonist. Tyramine also reduced the postganglionic discharges after preganglionic stimulation at 30 Hz for 2 sec in the presence of hexamethonium. The blockade of afterdischarges by tyramine was markedly reduced by phentolamine. Furthermore, tyramine was much less effective in blocking ganglia from reserpine-pretreated hamsters (6 mg/kg, 4 hr before isolation). Blockade of afterdischarges by norepinephrine was reduced by phentolamine, but not by reserpine. These results indicate that the blockade of afterdischarges with tyramine is mediated by endogenous catecholamines. The blocking action of tyramine was not reduced by cocaine (10(-5)M). Cocaine did reduce the afterdischarges, and this action of cocaine was partially antagonized by phentolamine and reserpine. These results suggest that the blockade of afterdischarges by tyramine and cocaine is due to inhibition of catecholamine uptake which potentiates the actions of endogenous catecholamines.

Action Potentials↗

PubMed1984

Tyramine pressor test: implications and limitations.

Tyramine, an indirectly acting sympathomimetic amine, can be used as a pharmacological tool to assess the peripheral adrenergic activity and its interactions with drugs in man. Of the various techniques used, the tyramine pressor test appears to be the most reliable method. It is convenient to perform and carries no significant morbidity, provided the subjects are selected carefully and the investigation is closely monitored. Basically, the tyramine pressor test involves measurement of systolic blood pressure in response to bolus intravenous tyramine injections. Tyramine sensitivity, which is taken as an index of peripheral adrenergic function, is defined as the amount of tyramine required to increase the systolic blood pressure by 30 mm of Hg and is determined from the dose response curve. Drugs which influence the adrenergic system are likely to alter the tyramine sensitivity. It provides valuable guidance regarding drug interactions and is useful in the assessment of certain neuropsychiatric conditions. However, since tyramine does not cross the blood brain barrier, information regarding only the peripheral effect is obtained.

Adolescent↗

PubMed1996

Tyramine pharmacodynamics during combined administration of lazabemide and moclobemide.

The objective of this study was to assess the tyramine pressor sensitivity during combined administration of selective and reversible inhibitors of monoamine oxidase A and B, viz. moclobemide (300 mg b.i.d.) and lazabemide (100 mg b.i.d.), respectively. In part A, 5 healthy male subjects underwent i.v. tyramine pressor tests before (baseline) and during (day 7) combined treatment with both drugs. The tyramine dose was titrated until an increase in systolic blood pressure of 30 mmHg was attained. Subsequently, lazabemide treatment was discontinued and i.v. tyramine pressor tests were again conducted after 2 - 3 days of moclobemide monotreatment. The tyramine pressor sensitivity factor (mean + or - SD) during combined moclobemide and lazabemide treatment was 4.2 + or - 0.9 and during moclobemide monotreatment 3.1 + or - 1.1. In part B, a separate panel of 8 subjects received combined treatment with moclobemide and lazabemide for up to 10 days. Ascending oral doses of tyramine were administered on days 7 - 10 to determine the threshold dose eliciting a 30 mmHg increase in systolic blood pressure. In comparison to baseline the effects of oral tyramine were potentiated by a factor of 13.5 + or - 6.9. The low amount of oral tyramine needed (51 + or - 20 mg) to induce relevant increases in blood pressure indicates that dietary precautions are needed when both MAO-A and B are inhibited by 2 reversible inhibitors.

Administration, Oral↗

PubMed1984

The tyramine challenge test as a marker for melancholia.

A previous study reported that unipolar depressives excrete significantly lower amounts of urinary tyramine-O-sulfate following oral administration of a tyramine hydrochloride load than do normal control subjects. This study replicates and extends those findings by showing that within the heterogeneous group of unipolar depressives, patients with melancholia and bipolar patients with a history of melancholia manifest a tyramine excretion deficit. A small subgroup of medication-free patients in remission from episodes of melancholia had abnormally low tyramine sulfate excretion levels while they were euthymic, supporting the suggestion that reduced tyramine sulfate excretion following oral tyramine loading is a trait marker for depression. Further study of the role of trace amines in affective illness is warranted. Clinical application is not warranted until further evaluation of the sensitivity, specificity, and reproducibility of this oral tyramine challenge test.

Adult↗

PubMed2005

Influence of the biogenic amine tyramine on ethanol-induced behaviors in Drosophila.

The biogenic amine tyramine has been implicated in drug-induced behavior. The Drosophila inactive mutant is characterized by reduced tyramine and octopamine levels and is defective in cocaine sensitization. To test whether there is an overlap in the use of the amine neurotransmitter system in ethanol- and cocaine-induced behaviors, mutant analyses were extended to the phenotypic characterization of inactive and other mutants effecting the tyramine and octopamine neurotransmitter system. The inactive mutant displays increased ethanol sensitivity and is impaired in the initial startle response upon ethanol application. Furthermore, this mutant fails to regulate its alcohol-induced hyperactivity properly. In contrast to the defects seen after cocaine application, inactive mutants develop normal ethanol tolerance and sensitize to the locomotor activating effect of ethanol. The tyramine-beta-hydroxylase mutant (TbetaH) with increased tyramine and depleted octopamine levels displays normal ethanol sensitivity, a startle repression, and hyperactivates more in response to ethanol. In addition, TbetaH mutants fail to develop a tolerance to the hyperactivating effect of ethanol. Ethanol-induced sensitization does not seem to be impaired in either mutant, suggesting that tyramine is not required for this process. The comparative analysis of the phenotypes associated with inactive and TbetaH mutants suggests that the fine tuning of ethanol-induced hyperactivity can be correlated with different tyramine levels. Defects in other aspects of ethanol-induced behaviors might be due to different molecules or mechanisms.

Animals↗

PubMed1996

The metabolism of tyramine by monoamine oxidase A/B causes oxidative damage to mitochondrial DNA.

Monoamine oxidases A/B (EC 1.4.3.4, MAO), flavoenzymes located on the outer mitochondrial membrane, catalyze the oxidative deamination of biogenic amines, such as dopamine, serotonin, and norepinephrine. In this study, we examined whether the H2O2 formed during the two-electron oxidation of tyramine [4-(2-aminoethyl)phenol] (a substrate for monoamine oxidases A/B) may contribute to the intramitochondrial steady-state concentration of H2O2 ([H2O2]ss) and, thus, be involved in the oxidative impairment of mitochondrial matrix components. Supplementation of intact, coupled rat brain mitochondria with benzylamine, beta-phenylethylamine, or tyramine showed initial rates of H2O2 production ranging from 0.4- to 1.6 nmol H2O2/min/mg protein. ESR analysis of the oxidative deamination of tyramine by intact rat brain mitochondria revealed the formation of hydroxyl (HO.) and carbon-centered radical adducts--the latter probably originating by the (HO.-)-mediated oxidation of mannitol. The signals were substantially enhanced upon addition of FeSO4 and were abolished by catalase. The intramitochondrial [H2O2]ss calculated in terms of glutathione peroxidase activity during the metabolism of tyramine was 48-fold higher (7.71 +/- 0.25 x 10(-7) M) than that obtained during the oxidation of succinate via complex II in the presence of antimycin A (1.64 +/- 0.2 x 10(-8) M). Oxidative damage to the brain mtDNA was assessed by single strand breakage. The ratio of nicked DNA for the preparations treated with tyramine and those without the amine was 1.5 +/- 0.29 (n = 4), 2.12 +/- 0.28 (n = 8, P < or = 0.05), and 3.12 +/- 0.69 (n = 3, P < or = 0.05) at 15, 30, and 60 min, respectively . Preincubation of mitochondria with tranylcypromine (trans-2-phenylcyclopropylamine), an inhibitor to MAO A/B, abolished mtDNA oxidative damage. Catalase inhibited mtDNA strand breakage by approximately 60%. Incubation of intact, coupled rat brain mitochondria with chlorodinitrobenzene (CDNB) depleted mitochondrial GSH by 72%. Tyramine-dependent damage of mtDNA was decreased by 68% in CDNB-treated mitochondria (with 28% remaining GSH). The [H2O2]ss was slightly increased in CDNB-treated mitochondria: 1.38- and 1.28-fold increase during the oxidation of succinate in the presence of antimycin A and during the oxidation of tyramine, respectively. These results suggest that the H2O2 generated during the MAO-catalyzed oxidation of biogenic amines and possibly certain neurotransmitters at the outer mitochondrial membrane contributes to the intramitochondrial [H2O2]ss and may cause oxidative damage to mtDNA. This is effected by the intramitochondrial concentration of GSH and might have potential implications for aging and neurodegenerative processes.

Animals↗