Cell Wall Changes and Partial Prevention of Fruit Softening in Prestorage Heat Treated ‘Anna’ Apples

The fermented food, whole meal Natto, viscous polymeric material from Natto, Natto bean, cooked soya bean, and 28 bacterial isolates from Natto were studied for their binding capacity to foodborne mutagenic-carcinogenic heterocyclic amines. The mutagenic heterocyclic amines used were Trp-P-1 (3-amino-1,4-dimethyl-5H-pyrido(4,3-b)indole); Trp-P-2 (3-amino-1-methyl-5H-pyrido(4,3-b)indole); Glu-P-1 (2-amino-6-methyldipyrido(1,2-a:3'2'-d)imidazole); PhIP (2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine); IQ (2-amino-3-methylimidazo(4,5-f)quinoline); MeIQ (2-amino-3,4-dimethylimidazo(4,5-f)quinoxaline); MeIQx (2-amino-3,8-dimethylimidazo(4,5-f)quinoxaline); and MeAαC (2-amino-3-methyl-9H-pyrido(2,3)indole). The lyophilized Natto and other fractions of Natto exhibited high binding activity towards Trp-P-1, Trp-P-2, PhIP, and MeAαC, while Glu-P-1, IQ, and MeIQ were not effectively bound. The binding capacity of bacterial isolates (Bacillus natto) were isolate-mutagen dependent. Heat treated lyophilized cells, cell wall, and cytoplasmic contents of the bacterial isolate with the highest binding capacity were analyzed for their ability to bind different heterocyclic amines. The results indicate the importance of the cell wall in binding to heterocyclic amines, whereas the cytoplasmic contents were less effective. Heat-treated cells were not much different from that of viable cells in their binding. The impact of different factors, such as pH, incubation time, metal ions, different concentrations of sodium chloride and alcohol, various enzymes, and acetylation of mutagens on binding of Trp-P-1 and IQ, were discussed. The significance of the present results is also discussed from the viewpoint that Natto, a fermented food, is able to scavenge dietary mutagenic heterocyclic amines through binding.Key words: fermented food, mutagens, heterocyclic amines, Natto, binding.

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Cell wall disassembly in ripening fruit

Functional Plant Biology ◽

10.1071/fp05234 ◽

2006 ◽

Vol 33 (2) ◽

pp. 103 ◽

Cited By ~ 434

Author(s):

David A. Brummell

Keyword(s):

Cell Wall ◽

Middle Lamella ◽

Primary Cell Wall ◽

Side Chains ◽

Fruit Softening ◽

Structure Degradation ◽

Wide Range ◽

Textural Changes ◽

Cell Wall Disassembly ◽

Pectin Solubilisation

Fruit softening during ripening involves a coordinated series of modifications to the polysaccharide components of the primary cell wall and middle lamella, resulting in a weakening of the structure. Degradation of polysaccharides and alterations in the bonding between polymers cause an increase in cell separation and a softening and swelling of the wall, which, combined with alterations in turgor, bring about fruit softening and textural changes. A wide range in the extent of cell wall pectic modifications has been observed between species, whereas the depolymerisation of xyloglucan is relatively limited and more consistent. The earliest events to be initiated are usually a loss of pectic galactan side chains and the depolymerisation of matrix glycans, which may begin before ripening, followed by a loss of pectic arabinan side chains and pectin solubilisation. The depolymerisation of pectins may begin during early to mid-ripening, but is usually most pronounced late in ripening. However, some of these events may be absent or occur at very low levels in some species. Cell wall swelling may be related to a loosening of the xyloglucan–cellulose network and to pectin solubilisation, and these processes combined with the loss of pectic side chains increase wall porosity. An increase in wall porosity later in ripening may allow increased access of degradative enzymes to their substrates.

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