热处理诱导采后柿果抗冷性机理的研究

【作者】 罗自生；

【导师】 席玙芳；

【作者基本信息】 浙江大学 ， 食品科学， 2002， 博士

【摘要】 本试验发现适当的热空气处理可诱导柿果的抗冷性。为此研究了热空气处理和对照(未处理)柿果在1℃下贮藏及20℃下后熟期间内源多胺含量、活性氧清除酶、脂氧合酶、脂肪酸组分含量、细胞壁水解酶、细胞壁组分含量及特性和细胞壁超微结构的变化规律，以探索热处理诱导柿果抗冷性的机理，结果如下： 柿果在12℃下可贮藏20—25天；在8℃下可贮藏35—45天；要贮藏50天以上，要求在4℃或以下的低温下贮藏。但柿果在低于4℃下贮藏20天后，移到常温下后熟时，又容易出现冷害症状，引起代谢失调和紊乱。表现为：外观色泽灰暗，有灰褐色斑点，局部凹陷、水渍状，严重果变黑；未成熟果实不能正常成熟软化；果肉风味平淡、褐变，局部发生果肉凝胶化(flesh gelling)；果汁粘稠，果肉出汁率降低。呼吸速率、乙烯释放量和果皮细胞膜透性异常增加。 适当的热空气处理减轻了柿果低温贮藏引起的冷害，其中以48℃热空气处理3小时和44℃热空气处理4小时的效果最佳，其冷害指数远低于对照。这两种处理均可抑制柿果呼吸速率、乙烯释放量和果皮细胞膜透性的上升；促进果实正常成熟软化，降低果汁相对粘度低，提高果肉出汁率，但对TTS含量影响较小。但柿果经52℃热空气处理2小时，容易引发热伤害，对果实贮藏反而不利。 柿果Spm、Spd和Put的积累水平与冷害的发生程度存在明显的负相关性，Spd(-0.923)＞Spm(-0.904)＞Put(-0.781)，Cad与冷害的关系不明显。热空气处理(48℃，3h)可以增加柿果内源多胺含量(Spd，Spm，Put，Cad)，减轻柿果冷害的发生。 柿果贮藏期间SOD、CAT、APX和GR活性降低，LOX活性增加。热空气处理(48℃，3h)延缓了CAT、APX和GR活性的降低，抑制了LOX活性的上升。 柿果冷藏期间脂肪酸各组分变化很小，当移至20C下后熟时，棕搁酸。硬脂酸和油酸的相对含量增加，亚油酸、亚麻酸和总不饱和脂肪酸的相对含量和 IUFA下降，促进冷害的发生。热空气处理（48 OC，3 h）延缓了亚油酸。亚麻酸和总不饱和脂肪酸的相对含量和 IUFA下降，以亚麻酸和总不饱和脂肪酸最为明显，延缓了冷害的发生。 柿果后熟软化与 PE、exoPG、endoPG、p－Gal、Xyl和 Cx活性上升有关。热处理柿果 endoFG、D－Gal和 Xyl活性明显高于对照；而PE、exo｛G和 Cx活性与对照柿果间无明显差异。冷害柿果无法正常软化与 endo－PG、p－Gal和 Xyl受到抑制，CSP、SSP和 ASH不能正常降解有关。 冷藏期间柿果的 CWM含量略有下降。当移到 20 C下成熟时，CWM含量迅速下降，热处理柿果的CWM含量明显低于对照。柿果冷藏期间细胞壁各组分含量和粘度均无明显变化。当移到20OC下成熟时，WSP含量迅速上升，热处理WSP含量明显高于对照。WSP相对粘度迅速下降，但热处理柿果的 WSP相对粘度低于对照。CSP、SSP、ASP和 ASH含量和相对粘度下降，热处理CSP、SSP、ASP和 ASH含量和相对粘度低于对照。柿果的 a－纤维素含量迅速下降，热处理a－纤维素含量低于对照。 柿果刚采收时，细胞壁结构完整，初生壁在中胶层的两边。在常温下后熟3天后，中胶层溶解，只剩下及少量排列松懈的微纤丝，初生壁局部被水解酶降解，甚至断裂。热处理柿果与正常成熟果类似，但中胶层溶解不完全，仍有大量微纤丝存在，但结构完整。冷害柿果细胞壁结构完整，初生壁加厚，中胶层少量溶解。 文中通过分析柿果冷害与内源多胺含量、活性氧清除酶、脂氧合酶、脂肪酸组分含量、细胞壁水解酶、细胞壁组分含量及特性和细胞壁超微结构的关系，对柿果冷害发生机理和热处理诱导柿果坑冷性机理进行了讨论。更多还原

【Abstract】 We found that heat treatment(48C,3h) can induce anti-chilling injury. In order to research the mechanism of HAT induction of anti-chilling injury in persimmon fruits, endogenous polyamines content, activated oxygen scavenging enzymes, LOX, fatty acid composition , cell wall hydrolase, cell wall composition and cell wall ultrastructure were investigated. Results are showed below:Persimmon fruits can store for 20-25 days and 35-45 days at 12C and 8C, respectively. If it is to be stored above 50 days, it must require a medium of 4C or below. Chilling injury symptoms and physiological disorders were observed when the fruits were transferred to normal temperature after storage at 4C for more than 20 days. As CI in persimmon is characterized by a brown-dark discoloration and pitting of the peel, the immature fruits cannot ripen normally,and fruit flesh lost flavor and even caused gelling of the flesh. Fruit juice had high viscosity and lower extractable juice rate. Respiration rate, ethylene production and permeability of persimmon fruits skin were abnormally high.Heat treatment reduced chilling sensitivity and alleviated physiological disorders. HAT at 48C for 3h or 44C for 4h were found to be most suitable foralleviating chilling injury in persimmon fruits. These two treatments retarded respiration rate, ethylene production and permeability of persimmon fruits skin. It also enhanced normal ripening and softening, reduced relative viscosity of fruit juice, improved extractable juice rate, but had little effect on TSS content. HT with too high temperature or too long exposure time caused heat injury. Persimmon fruits exposed to 52"C for 2h resulted in heat injury that was harmful to fruits.The extent of accumulation of spd, spm and put in persimmon correlated inversely with the occurrence chilling injury, Spd(-0.923) > Spm(-0.904) > Put(-0.781), respectively. Cad content did not correlate with chilling injury. HAT(48C,3h) increased endogenous polyamine(spd, spm, put and cad) contents, and reduced the occurrence of chilling injury. It has been suggested that these polyamines may protect plants from CI by a mechanism that involves protecting membrane lipids from peroxidation.The activities of SOD, CAT, APX and GR decrease during storage of persimmon, but the activities of LOX increased. HAT(48C,3h) retarded decrease in the activities of CAT, APX, GR and inhibited LOX from increasing.During cold storage of persimmon fruits there was very little change in fatty acid fraction, when returned to 20 C to ripen, the content of palmitic acid, stearic acid and oleic acid increased, while the content of linoleic acid, linolenic acid and total unsaturated fatty acid and IUFA decreased, giving rise to chilling injury syptoms. HAT(48C,3h) retarded decreases in the content of linoleic acid, linolenic acid, total unsaturated fatty acid and IUFA, especially linolenic acid and total unsaturated fatty acid, with concomitant retardation of chilling injury.The breaking down of persimmon fruit cell wall fractions such as pectin, hemicellulose and cellulose are caused by cell wall hydrolases such as PE, PG, P -Gal, Xyl and Cx. The activities of endo-PG, 0 -Gal and Xyl in HAT(48C,3h) fruits were significantly higher than control, and little or no differences among the activities of PE, exo-PG and Cx of heat treated and control fruits. In chilling injuried fruits endo-PG, P -Gal and Xyl were inhibited, and CSP, SSP ASP andASH could not be normally broken down, and fruits failed to ripening normally.CWM content of persimmon fruits declined little during cold storage. When returned to 20C to ripen, CWM content declined rapidly. The CWM content of HAT fruits was lower than that of control. There was little change in the cell wall composition content and relative viscosity during cold storage. When returned to 20C to ripen, WSP content increased rapidly, while the relative viscosity declined rapidly. WSP content of HAT was significantly higher than that of control, while WSP relative viscosity of HAT was signifi更多还原