Oral melanoma with osteocartilagineous differentiation: a case report and literature review.

Osteocartilagineous differentiation within malignant melanoma is a rare occurrence with several implications for diagnosis. Most of the reported cases have occurred in acral lentiginous malignant melanomas. In this paper, the authors describe the clinical, morphological, immunohistochemical features and surgical treatment of a case of primary oral mucosal melanoma with osteocartilaginous differentiation and they review the existing literature. The clinical history of a 67-year-old man affected of oral malignant melanoma was described from the first presentation to the second recurrence. FISH analysis on primary lesion and on relapses showed positive results both in epithelioid and in osteocondroblastic areas. Because of the scarcity of literature in osteogenic melanoma, histological identification may be problematic and prognostic factors and therapeutic protocols are nor well established. Immunohistochemical and molecular techniques can help to diagnosis this rare lesion.

Prevalence of thymidylate synthase gene 5'-untranslated region variants in an Argentinean sample.

Thymidylate synthase (TYMS) is a key enzyme in nucleotide synthesis and therefore, an important target of many chemotherapeutic agents. Expression of TYMS mRNA is thought to be modulated by a 28-bp tandem repeat polymorphism within its 5'-untranslated region, raising the question of this variant's utility in predicting the efficacy and toxicity of cancer treatment regimens. The aim of the present research was to describe the distribution of this TYMS polymorphism in the Argentinean population. A total of 199 randomly selected DNA samples from healthy volunteers were analyzed using polymerase chain reaction and polyacrylamide gel electrophoresis. The 2R and 3R alleles were present in 47.74 and 52.26% of samples, respectively, with frequencies of 21.6 (43), 52.3 (104), and 26.1% (52) recorded for the 2R/2R, 2R/3R, and 3R/3R genotypes, respectively. No significant difference regarding gender was observed. Our prevalence data are similar to those reported for other Caucasian populations. This opens a discussion concerning the reference population valid for comparisons and the clinical importance of this genotyping test as an additional tool in personalized medicine.

The signaling function of IDO1 incites the malignant progression of mouse B16 melanoma.

Indoleamine 2,3 dioxygenase 1 (IDO1), a leader tryptophan-degrading enzyme, represents a recognized immune checkpoint molecule. In neoplasia, IDO1 is often highly expressed in dendritic cells infiltrating the tumor and/or in tumor cells themselves, particularly in human melanoma. In dendritic cells, IDO1 does not merely metabolize tryptophan into kynurenine but, after phosphorylation of critical tyrosine residues in the non-catalytic small domain, it triggers a signaling pathway prolonging its immunoregulatory effects by a feed-forward mechanism. We here investigated whether the non-enzymatic function of IDO1 could also play a role in tumor cells by using B16-F10 mouse melanoma cells transfected with either the wild-type Ido1 gene (Ido1WT ) or a mutated variant lacking the catalytic, but not signaling activity (Ido1H350A ). As compared to the Ido1WT -transfected counterpart (B16WT), B16-F10 cells expressing Ido1H350A (B16H350A) were characterized by an in vitro accelerated growth mediated by increased Ras and Erk activities. Faster growth and malignant progression of B16H350A cells, also detectable in vivo, were found to be accompanied by a reduction in tumor-infiltrating CD8+ T cells and an increase in Foxp3+ regulatory T cells. Our data, therefore, suggest that the IDO1 signaling function can also occur in tumor cells and that alternative therapeutic approach strategies should be undertaken to effectively tackle this important immune checkpoint molecule.

A SOS3 homologue maps to HvNax4, a barley locus controlling an environmentally sensitive Na+ exclusion trait.

Genes that enable crops to limit Na(+) accumulation in shoot tissues represent potential sources of salinity tolerance for breeding. In barley, the HvNax4 locus lowered shoot Na(+) content by between 12% and 59% (g(-1) DW), or not at all, depending on the growth conditions in hydroponics and a range of soil types, indicating a strong influence of environment on expression. HvNax4 was fine-mapped on the long arm of barley chromosome 1H. Corresponding intervals of ∼200 kb, containing a total of 34 predicted genes, were defined in the sequenced rice and Brachypodium genomes. HvCBL4, a close barley homologue of the SOS3 salinity tolerance gene of Arabidopsis, co-segregated with HvNax4. No difference in HvCBL4 mRNA expression was detected between the mapping parents. However, genomic and cDNA sequences of the HvCBL4 alleles were obtained, revealing a single Ala111Thr amino acid substitution difference in the encoded proteins. The known crystal structure of SOS3 was used as a template to obtain molecular models of the barley proteins, resulting in structures very similar to that of SOS3. The position in SOS3 corresponding to the barley substitution does not participate directly in Ca(2+) binding, post-translational modifications or interaction with the SOS2 signalling partner. However, Thr111 but not Ala111 forms a predicted hydrogen bond with a neighbouring α-helix, which has potential implications for the overall structure and function of the barley protein. HvCBL4 therefore represents a candidate for HvNax4 that warrants further investigation.

Polystyrene nanoparticles may affect cell mitosis and compromise early embryo development in mammals.

A great interest surrounds the development of nanoparticles (NPs) for biomedical applications such as drug delivery and cancer therapy. However, the interplay between nanoscale materials and biological systems and the associated hazards have not been completely clarified yet. In this study, bovine oviductal epithelial cells (BOECs) and embryos were used as in vitro models to investigate whether cell mitosis and early mammalian embryo development could be affected by the exposure to polystyrene (PS) nanoparticles. Analysis of the karyotype performed on BOECs exposed to PS-NPs did not show chromosomal anomalies compared to the control, although more tetraploid metaphase plates were observed in the former. In vitro fertilization experiments designed to understand whether exposure to PS-NPs could affect pre-implantation development showed that incubation with PS-NPs decreased 8-cell embryo and blastocyst rate in dose-dependent fashion. The quality of the blastocysts in terms of mean cell percent blastomeres with fragmented DNA was the same in exposed blastocysts compared to controls. These results show that the exposure to PS-NPs may impair development. In turn, this may affect the rate of mitosis in embryos and yield a lower developmental competence to reach the blastocyst stage. This suggests that release in the environment and the subsequent accumulation of PS-NPs into living organisms should be carefully monitored to prevent cytotoxic effects that may compromise their reproduction rates.

An ALMT1 gene cluster controlling aluminum tolerance at the Alt4 locus of rye (Secale cereale L).

Aluminum toxicity is a major problem in agriculture worldwide. Among the cultivated Triticeae, rye (Secale cereale L.) is one of the most Al tolerant and represents an important potential source of Al tolerance for improvement of wheat. The Alt4 Al-tolerance locus of rye contains a cluster of genes homologous to the single-copy Al-activated malate transporter (TaALMT1) Al-tolerance gene of wheat. Tolerant (M39A-1-6) and intolerant (M77A-1) rye haplotypes contain five and two genes, respectively, of which two (ScALMT1-M39.1 and ScALMT1-M39.2) and one (ScALMT1-M77.1) are highly expressed in the root tip, typically the main site of plant Al tolerance/susceptibility. All three transcripts are upregulated by exposure to Al. High-resolution genetic mapping identified two resistant lines resulting from recombination within the gene cluster. These recombinants exclude all genes flanking the gene cluster as candidates for controlling Alt4 tolerance, including a homolog of the barley HvMATE Al-tolerance gene. In the recombinants, one hybrid gene containing a chimeric open reading frame and the ScALMT1-M39.1 gene each appeared to be sufficient to provide full tolerance. mRNA splice variation was observed for two of the rye ALMT1 genes and in one case, was correlated with a approximately 400-bp insertion in an intron.

Physical analysis of the complex rye (Secale cereale L.) Alt4 aluminium (aluminum) tolerance locus using a whole-genome BAC library of rye cv. Blanco.

Rye is a diploid crop species with many outstanding qualities, and is important as a source of new traits for wheat and triticale improvement. Rye is highly tolerant of aluminum (Al) toxicity, and possesses a complex structure at the Alt4 Al tolerance locus not found at the corresponding locus in wheat. Here we describe a BAC library of rye cv. Blanco, representing a valuable resource for rye molecular genetic studies, and assess the library's suitability for investigating Al tolerance genes. The library provides 6 x genome coverage of the 8.1 Gb rye genome, has an average insert size of 131 kb, and contains only ~2% of empty or organelle-derived clones. Genetic analysis attributed the Al tolerance of Blanco to the Alt4 locus on the short arm of chromosome 7R, and revealed the presence of multiple allelic variants (haplotypes) of the Alt4 locus in the BAC library. BAC clones containing ALMT1 gene clusters from several Alt4 haplotypes were identified, and will provide useful starting points for exploring the basis for the structural variability and functional specialization of ALMT1 genes at this locus.

Identification of a 2-propanol analogue modulating the non-enzymatic function of indoleamine 2,3-dioxygenase 1.

Indoleamine 2,3 dioxygenase 1 (IDO1) is a metabolic enzyme that catalyzes the conversion of the essential amino acid tryptophan (Trp) into a series of immunoactive catabolites, collectively known as kynurenines. Through the depletion of Trp and the generation of kynurenines, IDO1 represents a key regulator of the immune responses involved in physiologic homeostasis as well as in neoplastic and autoimmune pathologies. The IDO1 enzyme has been described as an important immune checkpoint to be targeted by catalytic inhibitors in the treatment of cancer. In contrast, a defective expression/activity of the enzyme has been demonstrated in autoimmune diseases. Beside its catalytic activity, the IDO1 protein is endowed with an additional function associated with the presence of two immunoreceptor tyrosine-based inhibitory motifs (ITIMs), which, once phosphorylated, bind SHP phosphatases and mediate a long-term immunoregulatory activity of IDO1. Herein, we report the screening of a focused library of molecules bearing a propanol core by a protocol combining microscale thermophoresis (MST) analysis and a cellular assay. As a result, the combined screening identified a 2-propanolol analogue, VIS351, as the first potent activator of the ITIM-mediated function of the IDO1 enzyme. VIS351 displayed a good dissociation constant (Kd = 1.90 µM) for IDO1 and a moderate cellular inhibitor activity (IC50 = 11.463 µM), although it did not show any catalytic inhibition of the recombinant IDO1 enzyme. Because we previously demonstrated that the enzymatic and non-enzymatic (i.e., ITIM-mediated) functions of IDO1 reside in different conformations of the protein, we hypothesized that in the cellular system VIS351 may shift the dynamic conformational balance towards the ITIM-favoring folding of IDO1, resulting in the activation of the signaling rather than catalytic activity of IDO1. We demonstrated that VIS351 activated the ITIM-mediated signaling of IDO1 also in mouse plasmacytoid dendritic cells, conferring those cells an immunosuppressive phenotype detectable in vivo. Thus the manuscript describes for the first time a small molecule as a positive modulator of IDO1 signaling function, paving the basis for an innovative approach to develop first-in-class drugs acting on the IDO1 target.

Mapping of seedling resistance in barley to Puccinia striiformis f. sp. pseudohordei.

The barley grass stripe rust (BGYR) pathogen Puccinia striiformis f. sp. pseudohordei was first detected in Australia in 1997. While studies have established that it is virulent on wild barley grass, and can infect several barley cultivars, the basis of genetic resistance to this pathogen in barley is largely unknown. Understanding the genetic basis of host resistance and ensuring the selection of germplasm with multiple resistance genes are important to mitigate the potential impact of BGYR in barley production. Genetic analysis of seedling resistance to BGYR in two barley doubled haploid populations, Amaji Nijo/WI2585 (AN/WI) and Galleon/Haruna Nijo (GL/HN), indicated that resistance is governed by several genes. Marker regression analysis of the seedling resistance data from the AN/WI population detected a major QTL, BGYR_WI1 (resistance contributed by WI2585 with the closest marker explaining 52 % of the total phenotypic effect) on chromosome 1HS, flanked by the loci Xabg59 and Xabc310b at map positions 0.0 and 6.9 cM, respectively. Similarly, a major QTL, BGYR_HN1, (resistance contributed by Haruna Nijo with the closest marker explaining 70 % of the total phenotypic effect) was detected in the GL/HN population and was mapped to 1HS, flanked by the loci Xbcd135 and XHOR1 at map positions 12.8 and 24.5 cM, respectively. In addition, several minor loci that provided resistance against BGYR were detected in both populations. While defined QTL intervals were large, the analysis nonetheless provides new information on sources of major QTL controlling resistance to BGYR.

Metabolite transport in isolated yeast mitochondria: fumarate/malate and succinate/malate antiports.

In this study, we investigated the metabolite permeability of isolated coupled Saccharomyces cerevisiae mitochondria. The occurrence of a fumarate/malate antiporter activity was shown. The activity differs from that of the dicarboxylate carrier (which catalyses the succinate/malate antiport) in (a) kinetics (Km and Vmax values are about 27 microM and 22 nmol min(-1) mg protein(-1) and 70 microM and 4 nmol min(-1) mg protein(-1), respectively), (b) sensitivity to inhibitors, (c) Ki for the competitive inhibitor phenylsuccinate and (d) pH profiles.

Saccharomyces cerevisiae mitochondria can synthesise FMN and FAD from externally added riboflavin and export them to the extramitochondrial phase.

Evidence is given that mitochondria isolated from Saccharomyces cerevisiae can take up externally added riboflavin and synthesise from it both flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD) probably due to the existence of the mitochondrial riboflavin kinase already reported and the novel mitochondria FAD synthetase. Moreover Saccharomyces cerevisiae mitochondria can export the newly synthesised flavin derivatives to the extramitochondrial phase. This has been proven to take place with 1:1 stoichiometry with riboflavin decrease outside mitochondria, thus showing that flavin traffic occurs across the mitochondrial membranes.

Repeated but not acute clomipramine decreases the effect of N-methyl-D-aspartate receptor activation on serotonergic transmission between the raphe nuclei and frontal cortex.

The effect of acute or repeated treatment with the antidepressant clomipramine (CIM) on N-methyl-D-aspartate (NMDA) evoked changes in extracellular 5-hydroxytryptamine (5-HT) in the raphe nuclei and frontal cortex of the same rat has been studied using microdialysis. Acute injection of CIM (10 or 20 mg/kg) caused an increase in raphe extracellular 5-HT but did not significantly alter extracellular 5-HT in the frontal cortex. Infusion of 25 microM NMDA into the raphe decreased extracellular 5-HT in this region and increased terminal extracellular 5-HT in the frontal cortex. In contrast, infusion of 100 microM NMDA into the raphe was followed by an increase in local dialysate 5-HT and a decrease in 5-HT release in the cortex. When NMDA infusion, at either 25 or 100 microM was preceded by one acute injection of CIM the effects of NMDA on 5-HT release in both brain structures were generally more marked than in vehicle injected controls. Repeated (15 day) treatment with CIM (10 or 20 mg/kg) caused a dose-dependent increase in basal extracellular 5-HT in both raphe and frontal cortex. In these animals, however, the effects of infusion of both 25 and 100 microM NMDA on 5-HT release in raphe and frontal cortex were greatly attenuated or abolished. This suggests that adaptive functional changes occur in NMDA receptor function during treatment with an antidepressant. The possible significance of this in the aetiology and treatment of depression is discussed.

Effects of imipramine on raphe nuclei and prefrontal cortex extracellular serotonin levels in the rat.

The effect of acute administrations of three doses of imipramine (1, 5 and 10 mg/kg s.c.), a widely used tricyclic antidepressant, on extracellular levels of serotonin (5-HT) has been studied by intracerebral microdialysis in raphe nuclei and prefrontal cortex of conscious rats. Imipramine 1 mg/kg s.c. did not change extracellular 5-HT in either raphe nuclei and prefrontal cortex. However, with the dose of 5 mg/kg s.c. imipramine induced in raphe nuclei, a brief increase of extracellular 5-HT followed by a lowering (55-65% basal release) of the neurotransmitter. The same dose of imipramine decreased (60-70% of basal value) extracellular 5-HT in prefrontal cortex. Imipramine 10 mg/kg s.c. significantly increased 5-HT levels in both raphe nuclei (190 +/- 20% above basal value) and prefrontal cortex (280 +/- 15% above basal value). Pretreatment with (-)pindolol (5 mg/kg s.c.), a non-selective 5-HT1A subtype receptor antagonist, 30 min before imipramine 5 mg/kg, modified the effect of the antidepressant: an increase, instead of a decrease, on prefrontal cortex dialysate 5-HT was observed. (-)Pindolol (10 mg/kg s.c.) increased extracellular 5-HT in both raphe nuclei (155 +/- 20% above basal value) and prefrontal cortex (160 +/- 8% above basal value). These data show that acute administration of imipramine modifies extracellular 5-HT at the level of the raphe nuclei and prefrontal cortex. 5-HT1A autoreceptors in the raphe nuclei, which this study suggests to be tonically active, may be stimulated after systemic administration of high doses of imipramine.

Mapping of the root lesion nematode ( Pratylenchus neglectus) resistance gene Rlnn1 in wheat.

The root lesion nematode, Pratylenchus neglectus, is an economically damaging pathogen of wheat and other crops. The development of P. neglectus-resistant wheat cultivars would be greatly accelerated through the use of molecular markers, as resistance phenotyping is extremely time-consuming. A greenhouse bioassay was developed to identify resistance phenotypes of doubled-haploid populations. Bulked-segregant analysis was used to identify AFLP markers linked to P. neglectus resistance in the wheat cultivar Excalibur. One resistance-linked AFLP marker was mapped close to chromosome 7A RFLP markers in a densely-mapped Cranbrook/Halberd population. One of the chromosome 7A RFLP probes, cdo347, was genotyped in the Tammin/Excalibur population segregating for response to root lesion nematode and showed 8% recombination with the P. neglectus resistance gene Rlnn1. The marker Xcdo347-7A was validated on Excalibur-and Krichauff-derived DH populations segregating for Rlnn1 and showed 14% and 10% recombination, respectively, with Rlnn1 in these populations.

N-methyl-d-aspartate receptors regulate 5-HT release in the raphe nuclei and frontal cortex of freely moving rats: differential role of 5-HT1A autoreceptors.

The effects of infusing N-methyl-d-aspartate (NMDA) into the raphe nuclei on release of 5-HT in this brain region and also the frontal cortex of the same animal were studied using in vivo microdialysis in freely moving rats. Infusion of 25 microM NMDA into the raphe led to a substantial decrease in dialysate 5-HT in this region and a prolonged increase in terminal 5-HT release in the frontal cortex. These effects were blocked by the specific NMDA receptor antagonist 2-amino-5-phosphonopentanoic acid (D-AP5; 100 microM). When 25 microM NMDA was co-infused into the raphe with the selective 5-HT1A receptor antagonist (N-¿2-¿4-(2-methoxyphenyl)-1-piperazinyl¿ethyl-N-(2-pyridinyl) cyclohexanecarboxamide) (WAY-100635; 1.0 microM) the effect of NMDA infusion was unaltered. WAY-100635 infused alone into the raphe did not alter local 5-HT or extracellular 5-HT in the cortex. Infusion of 100 microM NMDA into the raphe was followed by an increase in local dialysate 5-HT and a decrease in 5-HT release in the cortex. These changes were reversed by D-AP5. Following infusion of 100 microM NMDA with 1.0 microM WAY-100635 into the raphe local 5-HT release was still increased, however, the decrease in 5-HT observed in the frontal cortex was abolished. These data suggest that the degree of NMDA receptor activation leads to dramatically different outcomes with regard to serotonergic transmission to the frontal cortex. Furthermore, there appears to be a differential role of the 5-HT1A autoreceptor in regulating these effects. These data are discussed in relation to other studies on the regulation of serotonergic transmission in ascending pathways.

Chronic clomipramine administration reverses NMDA-evoked decreases in dopamine release in the raphe nuclei.

The effect of acute or chronic treatment with the antidepressant clomipramine (CIM) on basal and N-methyl-d-aspartate (NMDA) evoked release of dopamine (DA) in rat raphe has been studied using microdialysis. Acute injection of CIM (10 or 20 mg/kg) caused a decrease in raphe DA release, as did infusion of NMDA (25-100 microM) into this region. When NMDA infusion was preceded by a single acute injection of CIM no differences between NMDA and NMDA plus CIM treated groups was observed. Chronic (15 day) treatment with CIM caused a dose-dependent increase in basal extracellular DA. In addition the effect of infusing NMDA into the raphe on DA release was markedly reduced or abolished. This suggests that adaptive changes occur in NMDA receptor function during treatment with CIM.

Metabotropic and ionotropic glutamate receptors mediate opposite effects on periaqueductal gray matter.

Microinjections, into the dorso-lateral periaqueductal gray matter, of N-methyl-D-aspartic acid (NMDA, 0.07-7 nmol/rat) significantly (P < 0.01) increased arterial blood pressure in a dose-related manner. Pretreatment, 5 min before NMDA (7 nmol/rat), in the same area with 2-amino-5-phosphonovaleric acid (2-APV, 5 nmol/rat), a selective antagonist of NMDA receptors, significantly (P < 0.01) reduced NMDA-induced arterial hypertension. trans-(+/-)-1-Amino-1,3-cyclopentanedicarboxylic acid (t-ACPD, 6-30 nmol/rat), an agonist of metabotropic glutamate receptors (mGlu receptors), significantly (P < 0.01) decreased arterial blood pressure when microinjected into the dorsal-lateral periaqueductal gray matter. Pretreatment, 5 min before t-ACPD (30 nmol/rat), in the same area with L-2-amino-3-phosphono-propionate (L-AP-3, 30 nmol/rat), a putative antagonist of the mGlu receptors, was not able to prevent t-ACPD-induced hypotension. Microinjections of L-AP-3 (30 nmol/rat) induced a hypotension similar to the one obtained with t-ACPD at the dose of 6 nmol/rat. From these data we can suggest that mGlu receptors act inversely to the NMDA receptors in the dorso-lateral periaqueductal gray area and that L-AP-3 is a partial agonist rather than an antagonist of mGlu receptors within the periaqueductal gray area.

Chronic but not acute clomipramine alters the effect of NMDA receptor regulation of dopamine release in rat frontal cortex.

The effect of acute or chronic treatment with the antidepressant clomipramine (CIM) on N-methyl-D-aspartate (NMDA) evoked release of dopamine (DA) in the frontal cortex of the rat has been studied using microdialysis. Acute injection of CIM (10 or 20 mg/kg) caused a decrease in dialysate DA in the frontal cortex. Infusion of 25-100 microM NMDA into the frontal cortex decreased DA release in this region. When NMDA infusion was preceded by a single injection of CIM no marked differences between NMDA and NMDA + CIM treated groups were observed. Chronic (15 day) treatment with CIM (10 or 20 mg/kg) caused a dose-dependent increase in basal extracellular DA. In these animals, however, the effects of infusion of NMDA on DA release in the cortex were greatly attenuated or abolished. This suggests that adaptive changes occur in NMDA receptor function during treatment with an antidepressant. The possible significance of this in the aetiology and treatment of depression is discussed.

Involvement of opioid receptors in N-methyl-D-aspartate-induced arterial hypertension in periaqueductal gray matter.

Arterial hypertension induced by microinjections of N-methyl-D-aspartate (NMDA) (2 nmol/rat) into the midbrain periaqueductal gray matter was used to assess the involvement of opioid receptors (mu, delta and kappa) in modulating pressor periaqueductal gray neurons. Groups (n = 5-8) of urethane-anaesthetised rats received, 5 min before NMDA, microinjections of selective opioid receptor antagonists in the periaqueductal gray area and arterial blood pressure was monitored. Pretreatments with naloxone (5 nmol/rat), a non selective mu receptor antagonist, or naltrindole hydrochloride (5 nmol/rat), a selective delta receptor antagonist, significantly (P < 0.05) decreased by 31% and 37%, respectively, NMDA-induced hypertension. The latency for the maximum increase of NMDA-induced hypertension was also significantly (P < 0.05) increased with naloxone. Pretreatment with nor-binaltorphimine (5 nmol/rat), a selective kappa receptor antagonist, only increased the latency of NMDA-induced hypertension. Each opioid antagonist failed per se to alter arterial blood pressure. Microinjection of morphine (13 nmol/rat), a non selective mu receptor agonist, significantly decreased (P < 0.05) by 57.5% NMDA-induced arterial hypertension and this effect was antagonised by naloxone. Combined pretreatments in the periaqueductal gray area with naloxone and the GABAA antagonist bicuculline (2.5 nmol/rat; 5 min before naloxone) antagonised the effect of naloxone on NMDA-induced hypertension. In contrast, bicuculline significantly (P < 0.05) potentiated morphine-induced decrease of NMDA hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Increase of membrane permeability of mitochondria isolated from water stress adapted potato cells.

In order to gain some insight into mitochondria permeability under water stress, intact coupled mitochondria were isolated from water stress adapted potato cells and investigations were made of certain transport processes including the succinate/malate and ADP/ATP exchanges, the plant mitochondrial ATP-sensitive potassium channel (PmitoKATP) and the plant uncoupling mitochondrial protein (PUMP). The Vmax values measured for succinate/malate and ADP/ATP carriers, as photometrically investigated, as well as the same values for the PmitoK(ATP) and the PUMP were found to increase; this suggested that mitochondria adaptation to water stress can cause an increase in the membrane permeability.