Disturbances on Delta aminolevulinate dehydratase (ALA-D) enzyme activity by Pb2+, Cd2+, Cu2+, Mg2+, Zn2+, Na+, K+ and Li+: analysis based on coordination geometry and acid–base Lewis capacity

Pauza, N.L.; Cotti, M.J. Pérez; Godar, L.; Sancovich, A M Ferramola de; Sancovich, H. A.

doi:10.1016/j.jinorgbio.2004.10.013

Cited by 16 publications

(8 citation statements)

References 41 publications

(50 reference statements)

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“…4). 26,27 Indeed, agents that oxidize -SH groups, metals with high affinity for thiol groups or that compete with the Zn(II) binding site can inhibit δ-ALA-D. 20,[28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46] Fig. 1 Synthesis of porphobilinogen (PBG) from two 5-aminolevulinic acid (δ-ALA) molecules.…”

Section: δ-Aminolevulinate Dehydratase or Porporphobilinogen Synthase...mentioning

confidence: 99%

Aminolevulinate dehydratase (δ-ALA-D) as marker protein of intoxication with metals and other pro-oxidant situations

et al. 2012

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δ-ALA-D is a metalloenzyme that has 3 vicinal thiol/thiolate groups that coordinate with Zn(II). The proximity between the sulfhydryl groups renders δ-ALA-D extremely sensitive to oxidation by soft electrophiles, such as Pb(II), Hg(II), As(III) and organoseleno and organotellurium compounds. In fact, blood δ-ALA-D is a classical biomarker of lead exposure in humans. The inhibition of δ-ALA-D can increase the concentration of 5-aminolevulinate (δ-ALA), which is a pro-oxidant compound. δ-ALA can generate oxidative stress that can further increase δ-ALA-D inhibition. Recently, data have been obtained indicating that the δ-ALA-D could be a marker of oxidative stress in human pathologies. In summary, considering its high sensitivity to pro-oxidant situations, δ-ALA-D can be considered a universal marker of oxidative stress.

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Section: δ-Aminolevulinate Dehydratase or Porporphobilinogen Synthase...mentioning

confidence: 99%

Aminolevulinate dehydratase (δ-ALA-D) as marker protein of intoxication with metals and other pro-oxidant situations

et al. 2012

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“…They compete with other divalent cations such as Ca, Zn and Mg, replacing them, thus inhibiting their physiological roles (Pauza et al, 2005;Tabaldi et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Effect of cadmium on growth, micronutrient concentration, and δ-aminolevulinic acid dehydratase and acid phosphatase activities in plants of Pfaffia glomerata

Skrebsky¹,

Tabaldi²,

Pereira

et al. 2008

Braz. J. Plant Physiol.

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Pfaffia glomerata (Spreng.) Pedersen plantlets were grown under different cadmium (Cd) concentrations (0, 20, 40, 60 and 80 μM) in a hydroponic system during 7 d. Plant growth, micronutrient, chlorophyll and carotenoid concentrations, as well as δ-aminolevulinic acid dehydratase (ALA-D; E.C.4.2.1.24) and acid phosphatase (AP; E.C.3.1.3.2) activities were analysed. Cadmium concentration in both shoots and roots increased with increasing external Cd levels. Metal concentration in roots were on average 12-fold higher than in shoot tissues. Root length was unaffected by Cd treatments. In contrast, dry weight of both shoot and roots increased significantly after exposure to 20 and 40 μM Cd. Additionally, shoot and total plant dry weight were only reduced in plants exposed to 80 μM Cd. In contrast, root dry weight decreased significantly after exposure with Cd concentrations above 40 μM. A micronutrient-and organdependent response to Cd toxicity was observed. Zinc and Cu concentrations in both, shoot and roots did not alter due to exposure to Cd. Cadmium stress reduced Mn uptake but not its translocation within the plant. A synergistic effect of Cd on Fe concentration in root at 20 μM and 80 μM Cd levels was observed. The activity of AP, and especially that of ALA-D, was reduced with increasing Cd levels. At these Cd levels, the chlorophyll concentration was also reduced. There was a positive correlation between concentrations of carotenoids and chlorophylls. Our results indicate that P. glomerata seems to have some degree of Cd tolerance. parte aérea. O comprimento das raízes não foi afetado pelos tratamentos de Cd. Em contraste, a biomassa seca da parte aérea e raízes aumentou significativamente pela adição de 20 e 40 μM Cd. Além disso, a biomassa seca total das plantas somente diminuiu no nível de 80 μM Cd em relação à das plantas-controle. Por outro lado, a biomassa radicular diminuiu significativamente pela adição de Cd a níveis superiores a 40 μM. Constatou-se resposta dependente do órgão e do micronutriente à toxicidade de Cd. As concentrações de Zn e Cu na parte aérea e raízes não foram alteradas pela presença de Cd. A absorção de Mn foi diminuída pelo estresse de Cd, porém sua translocação não foi alterada. Um efeito sinergístico do Cd na concentração de Fe nas raízes foi observado nos níveis de 20 e 80 μM Cd. As atividades da ALA-D e AP foram diminuídas com o incremento dos níveis de Cd, porém a ALA-D foi mais afetada. Naquelas concentrações de Cd, a concentração de clorofila também foi diminuída. Houve uma correlação positiva entre as concentrações de carotenóides e clorofila. Os resultados indicam que a P. glomerata parece ter algum grau de tolerância ao Cd.palavras-chave: carotenóides, clorofilas, fitorremediação, ginseng brasileiro, micronutrientes, metal pesado.

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“…628 dehydratase (ALD), a key component of the hemeproducing machinery [7]. This triggers medical complications associated with iron metabolism and energy production [8,9].…”

Section: Introductionmentioning

confidence: 99%

Aluminum-Induced Mitochondrial Dysfunction Leads to Lipid Accumulation in Human Hepatocytes: A Link to Obesity

Mailloux¹,

Lemire²,

Appanna³

2007

Cell Physiol Biochem

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Mitochondrial dysfunction is the cause of a variety of pathologies associated with high energy-requiring tissues like the brain and muscles. Here we show that aluminum (Al) perturbs oxidative-ATP production in human hepatocytes (HepG2 cells). This Al-induced mitochondrial dysfunction promotes enhanced lipogenesis and the accumulation of the very low density lipoprotein (VLDL). Al-stressed HepG2 cells secreted more cholesterol, lipids and proteins than control cells. The level of apolipoprotein B-100 (ApoB-100) was markedly increased in the culture medium of the cells exposed to Al. ¹³C-NMR and HPLC studies revealed a metabolic profile favouring lipid production and lowered ATP synthesis in Al-treated cells. Electrophoretic and immunoblot analyses pointed to increased activities and expression of lipogenic enzymes such as glycerol 3-phosphate dehydrogenase (G3PDH), acetyl CoA carboxylase (ACC) and ATP-citrate lyase (CL) in the hepatocytes exposed to Al, and a sharp diminution of enzymes mediating oxidative phosphorylation. D-Fructose elicited the maximal secretion of VLDL in the Al-challenged cells. These results suggest that the Al-evoked metabolic shift favours the accumulation of lipids at the expense of oxidative energy production in hepatocytes.

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Disturbances on Delta aminolevulinate dehydratase (ALA-D) enzyme activity by Pb2+, Cd2+, Cu2+, Mg2+, Zn2+, Na+, K+ and Li+: analysis based on coordination geometry and acid–base Lewis capacity

Cited by 16 publications

References 41 publications

Aminolevulinate dehydratase (δ-ALA-D) as marker protein of intoxication with metals and other pro-oxidant situations

Aminolevulinate dehydratase (δ-ALA-D) as marker protein of intoxication with metals and other pro-oxidant situations

Effect of cadmium on growth, micronutrient concentration, and δ-aminolevulinic acid dehydratase and acid phosphatase activities in plants of Pfaffia glomerata

Aluminum-Induced Mitochondrial Dysfunction Leads to Lipid Accumulation in Human Hepatocytes: A Link to Obesity

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