Ethanol production and toxicity in suspension-cultured carrot cells and embryos

Perata, Pierdomenico; Loschiavo, F; Alpi, Amedeo

doi:10.1007/bf00401019

Cited by 29 publications

(18 citation statements)

References 22 publications

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“…1 b). This response indicated a root oxygen deficiency in plants grown in the hypoxic media and the potential for alcoholic fermentation (Smith and ap Rees 1979;Keeley 1979;Perata et al 1988) (Fig. lb).…”

Section: Discussionmentioning

confidence: 95%

Mechanism for the hydrogen sulfide‐induced growth limitation in wetland macrophytes

Koch

Mendelssohn

McKee

1990

Limnology & Oceanography

302

162

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Hydrogen sulfide, a phytotoxin that often accumulates in anoxic marine and freshwater marsh soils, suppressed the activity of alcohol dehydrogenase (ADH), the enzyme that catalyzes the terminal step in alcoholic fermentation, in the roots of two wetland macrophytes. This inhibition of root ADH activity with increasing sulfide concentration was associated with decreases in root total adenine nucleotide pool (ATP + ADP + AMP), the adenylate energy charge ratio (AEC), nitrogen uptake (percent recovery of rSNH,+-N) and growth (leaf elongation). These responses were species-specific with a greater negative impact in the freshwater marsh species that naturally inhabits low-sulfide environments. These findings lend support to the hypotheses that ADH activity, as a mcasurc of fermcntative metabolism, is important in maintaining the root energy status of wetland plants under hypoxic-anoxic conditions, that there is a significant negative effect of H,S on the anoxic production of energy in these roots, and that an important negative effect of H,S on plant growth is an inhibition of the energy-dependent process of N uptake.

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Section: Discussionmentioning

confidence: 95%

Mechanism for the hydrogen sulfide‐induced growth limitation in wetland macrophytes

Koch

Mendelssohn

McKee

1990

Limnology & Oceanography

302

162

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“…In 1971, McManmon and Crawford (13) suggested that the diversification of the end products of fermentive metabolism could explain flooding tolerance in some species. Jackson et al (9) questioned whether ethanol itself could be responsible for anoxic injuries, but we (17,18) later demonstrated that ethanol can be toxic to specific plant systems even at concentrations comparable to those commonly found in plant tissues subjected to oxygen deficit.…”

mentioning

confidence: 86%

“…As part of our work concerning ethanol toxicity to plants (2,(15)(16)(17)(18), we report the presence of reaction products of acetaldehyde with carrot cell proteins. We used an immunological approach, with the aim of verifying the presence of such conjugates in relation to the induction of injuries to ethanol-treated carrot cells.…”

mentioning

confidence: 99%

Immunological Detection of Acetaldehyde-Protein Adducts in Ethanol-Treated Carrot Cells

Perata¹,

Vernieri²,

Armellini³

et al. 1992

Plant Physiol.

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Polyclonal antibodies able to recognize protein-acetaldehyde conjugates were produced and characterized. The antibodies react with sodium cyanoborohydride-reduced Schiff's bases between acetaldehyde and a protein, independently of the nature of the macromolecule binding the acetaldehyde moiety. Only conjugates between acetaldehyde or propionaldehyde and a protein are recognized; conjugates obtained with other aldehydes are not reactive. Results conceming the formation of acetaldehyde adducts with carrot (Daucus carota L.) proteins are presented as well as the presence of such conjugates in ethanoltreated carrot cell cultures, a system highly sensitive to the presence of ethanol in the culture medium.

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“…The process of carrot somatic embryogenesis is almost completely arrested by the addition of ethanol to the culture medium (Perata et al, 1988). The concentration of AA that inhibits cell growth is 40-fold lower than the concentration of ethanol that has a similar affect.…”

mentioning

confidence: 99%

Acetaldehyde Is a Causal Agent Responsible for Ethanol-Induced Ripening Inhibition in Tomato Fruit

1997

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Inhibition of tomato (Lycopersicon esculentum Mill.) fruit ripening by exogenously applied ethanol was shown to be caused by elevated endogenous levels of acetaldehyde (AA). Exposure of excised pericarp discs of mature-green tomato fruit to ethanol or AA vapors produced elevated levels of both compounds in the tissue, but only the levels of AA were associated with ripening inhibition. Ripening inhibition was dependent on both the applied concentration and the duration of exposure. Discs treated with inhibitory levels of AA had levels of ethanol that were elevated but below that associated with inhibition of ripening. The in vivo activity of alcohol dehydrogenase was inhibited 40 to 60% by 4-methylpyrazole (4-MP), a competitive inhibitor of this enzyme. The inhibitory effect of ethanol on ripening was reduced by the simultaneous application of 4-MP. Tissue treated with 4-MP plus AA vapors had higher endogenous levels of AA and ripening was inhibited longer than in tissue without 4-MP. The tissue AA level resulting from ethanol or AA application appears to be the critical determinant of ripening inhibition.

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Ethanol production and toxicity in suspension-cultured carrot cells and embryos

Cited by 29 publications

References 22 publications

Mechanism for the hydrogen sulfide‐induced growth limitation in wetland macrophytes

Mechanism for the hydrogen sulfide‐induced growth limitation in wetland macrophytes

Immunological Detection of Acetaldehyde-Protein Adducts in Ethanol-Treated Carrot Cells

Acetaldehyde Is a Causal Agent Responsible for Ethanol-Induced Ripening Inhibition in Tomato Fruit

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