Effects of Lovastatin treatment on ethylene production, α-farnesene biosynthesis, and scald development were studied using `Delicious' and `Granny Smith' apples [Malus sylvestris (L.) Mill. var. domestica (Borkh.) Mansf.] and `d'Anjou' pears (Pyrus communis L.) stored in air at 0 °C. During 6 months storage, Lovastatin did not affect internal ethylene concentration but reduced α-farnesene production in a concentration dependent manner in both apples and pears. Lovastatin reduced scald at 0.63 mmol·L-1 and inhibited scald completely at 1.25 or 2.50 mmol·L-1 in `Delicious' and `Granny Smith' apples. In `d'Anjou' pears, Lovastatin at concentrations from 0.25 to 1.25 mmol·L-1 inhibited scald completely. After 8 months storage, inhibition of scald in both apples and pears by Lovastatin was concentration-dependent but none of the concentrations totally eliminated scald. Compared with 11.8 mmol·L-1 diphenylamine, Lovastatin treatment reduced scald to the same level at 1.25 mmol·L-1 in `d'Anjou' pear and 2.50 mmol·L-1 in `Delicious' and `Granny Smith' apples. Lovastatin did not affect apple or pear fruit color, firmness, soluble solids content, or titratable acidity during storage in either apple or pear compared with the controls. Chemical name used: [1S-[1a (R °), 3α, 7β, 8β (2S °, 4S °), 8αβ]]-1,2,3,7,8,8α-hexahydro-3,7-dimethyl-8-[2-(tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl)ethyl]-1-naphthaienyl 2-methylbutanoate (Lovastatin).
Effects of α-farnesene biosynthesis precursors on α-farnesene and ethylene production were studied using Lovastatin-treated or nontreated `Delicious' and `Granny Smith' apples [Malus sylvestris (L.) Mill. var. domestica (Borkh.) Mansf.]. In nontreated fruit, α-farnesene was detected only in fruit peel (≈3 mm) and not in the more proximal cortical tissue. α-Farnesene was not detectable in preclimacteric fruit peel at harvest. Mevalonic acid lactone (MAL) or farnesyl pyrophosphate (FPP) induced α-farnesene production when fed to preclimacteric peel tissue, but hydroxymethylglutaric acid (HMG) did not. Fruit stored at 0 °C for 30 days (climacteric fruit) produced α-farnesene, and addition of HMG, MAL, or FPP further increased α-farnesene production. When treated at harvest with Lovastatin at 1.25 mmol·L-1 and stored at 0 °C for 30 days, fruit produced ethylene but did not produce α-farnesene. Whereas MAL and FPP induced α-farnesene production in peel sections from these fruit, HMG did not. Induction of α-farnesene by precursor feeding was concentration-dependent and had no effect on ethylene production. Cortical tissue sections from climacteric fruit did not produce α-farnesene unless HMG, MAL, or FPP were fed during incubation. Including Lovastatin at 0.63 mmol·L-1 in the feeding solution eliminated HMG induced α-farnesene production, but did not affect MAL or FPP-induced α-farnesene production. Neither precursor feeding nor Lovastatin treatment affected ethylene production in cortical tissues. Chemical name used: [1S-[1a (R°), 3α, 7β, 8β (2S°, 4S°), 8αβ]]-1,2,3,7,8,8α-hexahydro-3,7-dimethyl-8-[2-(tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl)ethyl]-1-naphthalnyl 2-methylbutanoate (Lovastatin).
Lovastatin is a specific hydroxymethylglutaryl coenzyme-A reductase inhibitor in animals and as such, is a potent cholesterol lowering pharmaceutical for human use. Because it has also been shown to inhibit α-farnesene in certain plants, we investigated its effects on ethylene and α-farnesene biosynthesis, volatile production, and fruit color during ripening in `Golden Supreme' apples [Malus sylvestris (L.) Mill. var. domestica (Borkh.) Mansf.]. Immediately after harvest, fruit were dipped in Lovastatin solution for 2 min, allowed to dry, and stored in the dark at 20 °C for 30 days. Internal ethylene at harvest was low (< 0.1 mL·L-1) and α-farnesene was undetectable. Both internal ethylene and α-farnesene increased in nontreated fruit during 30 days storage. Prestorage Lovastatin treatment did not affect ethylene synthesis, but at 1.25 or 2.5 mmol·L-1 nearly eliminated α-farnesene production. At 0.25 mmol·L-1, Lovastatin delayed the increase in α-farnesene production about 12 days and reduced total α-farnesene production by the end of storage compared with controls. When applied to nontreated preclimacteric fruit, ethephon at 1.4 mmol·L-1 increased both internal ethylene concentration and α-farnesene production. In Lovastatin-treated preclimacteric fruit, however, ethephon increased internal ethylene concentration without promoting α-farnesene synthesis. In another trial, after 30 days storage at 0 °C, fruit were treated with 1.25 mmol·L-1 Lovastatin and stored at 20 °C with air circulation for 20 days. These fruit accumulated similar amounts of ethylene as nontreated controls, but α-farnesene production decreased rapidly and was not detectable after 5 days. Treating with ethephon at 1.4 mmol·L-1 increased α-farnesene production in control fruit but not in Lovastatin-treated fruit. Lovastatin treatment did not affect the change in fruit color. Chemical names used: [1S-[1α (R °), 3α, 7β, 8β (2S °, 4S °), 8ab]]-1,2,3,7,8,8α-hexahydro-3,7-dimethyl-8-[2-(tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl)ethyl]-1-naphthaienyl 2-methylbutanoate (Lovastatin); 2-chloroethylphosphonic acid (ethephon).
In late September of 1981 and 1982, eight-year-old ‘Oregon-spur Delicious’ apple (Malus domestica) trees on M7 rootstock were sprayed immediately after harvest with 500 ppm AVG. The following spring of both years the number of spur leaves and lateral shoots on one-year-old wood was increased on treated trees. Total N was reduced and sucrose and fructose were increased in dormant one-year-old shoots of AVG-treated trees. Cold hardiness was not affected. Throughout the dormant period both apical and one-year-old lateral buds excised from treated trees and incubated in the dark at 24°C produced less ethylene over a period of 24 hr than buds from untreated trees. In situ ethylene production from apical buds of treated trees was also reduced as growth resumed in the spring. Chemical name used: N-(phenylmethyl)-lH-purin-6-amine (AVG).
Preclimacteric `Bartlett' pears (Pyrus communis L.) were dipped for 3 min in either corn (Zea mays L.) or soybean [(Glycine max (L.) Merrill] oil emulsion immediately after harvest and stored at 0 °C. Untreated control fruit developed higher percentages of senescent scald, core breakdown, and decay after 15 weeks storage. Both treatments inhibited senescent scald, core breakdown, and decay in a similar and concentration dependent manner. Complete control of senescent scald and core breakdown was achieved by emulsions at 5% and 10%, and of decay by emulsion at 10%. Compared with controls, emulsion treatments delayed and reduced internal ethylene accumulation and volatile production in early storage and increased them in late storage. Compared with controls, fruit treated with oil contained similar levels of internal O2 and CO2 in early storage and higher CO2 and lower O2 in late storage. While control fruit lost commercial value after 15 weeks at 0 °C plus 5 days at 20 °C, oil-treated fruit exhibited normal color change, and had higher soluble solids, titratable acidity, and volatile production. Microscopic examination revealed that emulsion-treated fruit had a continuous surface film conforming to the contour of the fruit.