A theoretical approach on the role of fermentation in harvested plant products
A theoretical approach on the role of fermentation in harvested plant products
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关于发酵在收获的植物产品中的作用的理论方法
DOI：
10.17660/actahortic.1998.464.58
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
J. Oosterhaven
中科院分区：
文献类型：
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作者：
H. Peppelenbos;J. Oosterhaven
大多数关于气调储存 (CA) 和气调包装 (MA) 的研究都强调最佳气体浓度，定义为在不引入组织紊乱的情况下产品质量变化几乎停止的浓度。它们取决于产品对低 O2 浓度 [O2] 的耐受性，通常在 1–4␘2 范围内。对这些条件的耐受性似乎取决于物种和组织特异性的形态和代谢适应（Ratcliffe，1995）。在氧气限制期间，能量代谢从呼吸转变为发酵，导致组织坏死和变色、异味和异味等疾病（Kader 等，1989），表明它们之间存在直接关系。 Kader (1986) 指出，丙酮酸脱羧为乙醛直至乙醇，会导致异味的产生和组织分解。事实上，当呼吸速率降低而不发生发酵时，[O2] 通常被认为是最佳的（Banks 等，1993）。因此，传统上对CA的研究一直集中在避免发酵上。曾经有过三个概念；灭绝点（EP，Blackman，1928）、无氧补偿点（ACP，Boersig 等，1988）和呼吸商断点（RQB，Gran 和 Beaudry，1993）。所有这些都与发酵速率有关。 EP 是最高的[O2]，没有无氧代谢，以乙醇或乙醛的产生来衡量。然而，乙醇现在被检测为苹果和许多其他在有氧条件下保存的水果的正常成分（Boersig等人，1988；Ke等人，1990，1993；Colelli等人，1991；Nanos等人，1992），因此EP是一个站不住脚的概念（Boersig等人，1988）。 ACP，即 CO2 生成量最小时的 [O2]，可以解释为无氧 CO2 生成量的增加补偿了好氧 CO2 生成量的减少的 [O2]。这意味着无氧代谢的 [O2] 高于 ACP。 RQB 是[O2]，其中当[O2] 进一步降低时RQ 增加。 ACP 和 RQB 与发酵速率没有直接关系，而是由气体交换速率得出。 ACP 和 RQB 都接受发酵速率的一定增加，以二氧化碳产量或 RQ 的增加来衡量。由于发酵在假定的最佳浓度下活跃，即使在正常空气中，也不清楚是否存在阻止发酵的[O2]。因此，发酵本身的发生不能作为选择最佳储存浓度的标准。多年来，对于发酵增加与组织疾病之间的相关性，出现了两种可能的解释：（1）发酵代谢物的毒性作用； (2)能源生产不足以满足能源需求。我们将讨论存储过程的生理相关性和影响。发酵代谢物的毒性作用：发酵代谢物通常被认为是与其相关的储存障碍的原因。许多关于植物组织在缺氧条件下存活的代谢研究都集中在主要发酵终产物乳酸、乙醛和乙醇的可能毒性上（Perata 和 Alpi，1993；Ricard 等，1994）。乳酸 - 在许多植物中，乳酸的形成先于乙醇的产生。戴维斯等人。 (1974) 因此提出，在从氧化途径转变为发酵途径的过程中，乳酸通过降低细胞 pH 值从而增加 ADH 活性来发挥调节作用。然而，不同的研究人员发现乳酸的产生与细胞质 pH 值的最初下降并不完全匹配（Ratcliffe，1995）。此外，在诱导酒精发酵之前发生乳酸发酵并不普遍存在于植物中（Perata 和 Alpi，1993）。尽管如此，细胞质 pH 值的调节被认为是
Most research on controlled atmosphere storage (CA) and modified atmosphere packaging (MA) places emphasis on optimal gas concentrations, defined as the concentrations where quality change of a product almost ceases without introduction of tissue disorders. They depend on the tolerance of products to low O2 concentrations [O2], often, in the range of 1–4␘2. Tolerance to these conditions appears to depend on both morphological and metabolic adaptations that are both species and tissue specific (Ratcliffe, 1995). During O2 limitation, energy metabolism switches from respiration to fermentation leading to disorders like necrotic and discoloured tissues, off odours and off tastes (Kader et al., 1989), suggesting that they have a direct relationship. Kader (1986) stated that decarboxylation of pyruvate to acetaldehyde through to ethanol results in the development of off-flavours and tissue breakdown. In fact [O2] is often considered to be optimal when respiration rates are reduced without development of fermentation (Banks et al., 1993). Therefore, traditionally, research on CA has been focused on avoiding fermentation. There have been three concepts; the Extinction Point (EP, Blackman, 1928), the Anaerobic Compensation point (ACP, Boersig et al., 1988) and the Respiration Quotient Breakpoint (RQB, Gran and Beaudry, 1993). All are related to fermentation rates. The EP is the highest [O2] with no anaerobic metabolism, measured as ethanol or acetaldehyde production. However, ethanol is now detected as a normal constituent of apples and many other fruits held under aerobic conditions (Boersig et al., 1988; Ke et al., 1990, 1993; Colelli et al., 1991, Nanos et al., 1992), so that the EP is therefore an untenable concept (Boersig et al., 1988). The ACP, the [O2] at which CO2 production is minimal, can be explained as the [O2] where an increase in anaerobic CO2 production compensates for the decrease in aerobic CO2 production. This implies anaerobic metabolism at higher [O2] than the ACP. The RQB is the [O2] where the RQ increases when [O2] is further lowered. The ACP and the RQB are not directly related to fermentation rates but are derived from gas exchange rates. Both the ACP and the RQB accept a certain increase in fermentation rate, measured as an increased CO2 production or RQ. With fermentation active at supposed optimal concentrations, and even in normal air, it is unclear whether there is an [O2] which precludes fermentation. Therefore occurrence of fermentation itself cannot be a criterion for selecting optimal storage concentrations. Throughout the years two possible explanations arose for the correlation between increased fermentation and tissue disorders: (1), a toxic effect of fermentative metabolites; (2), insufficient energy production to cover energy demands. We will discuss the physiological relevance and implications for storage procedures. Toxic effect of fermentative metabolites: Fermentative metabolites are often considered to be the cause of storage disorders with which they are often associated. Many metabolic studies of the survival of plant tissues in the absence of oxygen are focused on the possible toxicity of the main fermentation end-products, lactic acid, acetaldehyde and ethanol (Perata and Alpi, 1993; Ricard et al., 1994). Lactic acid - In many plants, formation of lactate precedes ethanol production. Davies et al. (1974) therefore proposed a regulatory role for lactate during the shift from oxidative to fermentative pathways, through decreasing cell pH and thereby increasing ADH activity. Different researchers, however, have found that the production of lactate is not well matched with the initial fall in the cytoplasmatic pH (Ratcliffe, 1995). Also the occurrence of lactic fermentation prior to the induction of alcoholic fermentation is not universally present in plants (Perata and Alpi, 1993). Nonetheless, the regulation of cytosolic pH is considered to be the