Involvement of Jasmonic Acid in Elicitor-Induced Phytoalexin Production in Suspension-Cultured Rice Cells.

It has been suggested that jasmonic acid (JA) could be an integral part of a general signal transduction system regulating inducible defense genes in plants. It was reported that treatment with an elicitor (N-acetylchitoheptaose) induced production of phytoalexin in suspension-cultured rice (Oryza sativa L.) cells. In this study, the role of JA in the induction of phytoalexin production by N-acetylchitoheptaose was investigated. Exogenously applied ([plus or minus])-JA (10-4 M) clearly induced the production of momilactone A, a major phytoalexin, in suspension-cultured rice cells. On the other hand, in rice cells treated with N-acetylchitoheptaose, endogenous JA was rapidly and transiently accumulated prior to accumulation of momilactone A. Treatment with ibuprofen, an inhibitor of JA biosynthesis, reduced production of momilactone A in the cells treated with N-acetylchitoheptaose, but the addition of ([plus or minus])-JA increased production of momilactone A to levels higher than those in the elicited rice cells. These results strongly suggest that JA functions as a signal transducer in the induction of biosynthesis of momilactone A by N-acetylchitoheptaose in suspension-cultured rice cells.

Phytoalexin production by amino acid conjugates of jasmonic acid through induction of naringenin-7-O-methyltransferase, a key enzyme on phytoalexin biosynthesis in rice (Oryza sativa L.).

Amino acid conjugates of jasmonic acid are found to elicit production of the flavonoid phytoalexin, sakuranetin in rice leaves. The elicitation is shown to arise from induction of naringenin 7-O-methyltransferase, a key enzyme of sakuranetin biosynthesis. The (-)-phenylalanine conjugate, one of the active compounds, is characterized by high activity for both sakuranetin and enzyme induction and low phytotoxicity against rice growth. Both (+)-enantiomers of the conjugates and free amino acids do not show any activity. The amino acid conjugate of jasmonic acid is speculated to be the later component in the signaling transduction chain in stressed rice plants.

Phytoalexin production elicited by exogenously applied jasmonic acid in rice leaves (Oryza sativa L.) is under the control of cytokinins and ascorbic acid.

Jasmonic acid (JA) has been shown to be a signaling compound which elicits the production of secondary metabolites including phytoalexins in plants. It has been shown that the phytoalexin production is elicited by exogenously applied JA in rice leaves. We now show that this phytoalexin production by exogenously applied JA is significantly counteracted by cytokinins, kinetin and zeatin. Kinetin and zeatin also inhibit the induction of naringenin-7-O-methyltransferase (a key enzyme in rice phytoalexin production) by JA. A natural free radical scavenger, ascorbic acid (AsA) shows both counteractive and enhancing effects on JA-inducible phytoalexin production, depending on its concentration. This effect of AsA suggests that active oxygen species (AOS) may play important roles in phytoalexin production by JA in rice leaves.

Coronatine elicits phytoalexin production in rice leaves (Oryza sativa L.) in the same manner as jasmonic acid.

The phytotoxin coronatine induced the accumulation of the flavonoid phytoalexins sakuranetin and momilactone A in rice leaves. Coronatine-inducible sakuranetin production was under the control of kinetin and ascorbic acid (AsA), as observed with jasmonic acid (JA). The effects of kinetin and AsA on the activity of coronatine indicated that coronatine might elicit sakuranetin production in a manner similar to JA. The similarity of both their structures and the manner of elicitation of coronatine and JA suggest that they might interact at the same active site(s) to lead to phytoalexin production.

Induced accumulation of 2-hydroxy-4,7-dimethoxy-1,4-benzoxazin-3-one glucoside (HDMBOA-Glc) in maize leaves.

Accumulation of 2-(2-hydroxy-4,7-dimethoxy-1,4-benzoxazin-3-one)-beta-D-glucopyranose (HDMBOA-Glc) was induced in maize leaves by treatment with CuCl2, chitopentaose, penta-N-acetylchitopentaose, or jasmonic acid (JA). The accumulation of HDMBOA-Glc was accompanied by a decrease in level of 2-(2,4-dihydroxy-7-methoxy-1,4-benzoxazin-3-one)-beta-D-glucopyranose (DIMBOA-Glc). When the leaf segments were treated with JA in the presence of [Me-2H3]L-methionine, the label was efficiently incorporated into HDMBOA-Glc, while no incorporation into DIMBOA-Glc or HMBOA-Glc was detected, suggesting the conversion of constitutive DIMBOA-Glc to HDMBOA-Glc by methylation at the 4-position. Levels of endogenous JA and its leucine conjugate transiently increased prior to the accumulation of HDMBOA-Glc in leaf segments treated with CuCl2 and chitopentaose. The lipoxygenase inhibitor ibuprofen suppressed the accumulation of HDMBOA-Glc induced by CuCl2 treatment, and the reduced accumulation of HDMBOA-Glc was recovered by addition of JA. These findings suggested that JA functions as a signal transducer in the induction of HDMBOA-Glc accumulation.

[Rare intra-abdominal complications of a ventriculoperitoneal shunt: report of three cases].

Three cases of rare intra-abdominal complications of ventriculoperitoneal shunt (VPS) surgery are reported. Case 1 was a 32-year-old male who had undergone VPS surgery for hydrocephalus following meningitis on July 10, 1980. Two weeks later he developed fever and a cystic mass about 10 cm in diameter in the right hypochondrium. Shuntography and a barium enema study demonstrated a pseudocyst at the distal end of the shunt. The cyst wall was excised, the peritoneal tube removed, and VPS converted to a ventriculoatrial route following which the pseudocyst resolved. Case 2 was a 49-year-old female who developed hydrocephalus following subarachnoid hemorrhage, and VPS surgery was performed on March 10, 1989. Two weeks later, she developed fever and right upper abdominal pain. Abdominal x-ray and CT scan revealed a right subdiaphragmatic abscess. The abscess was drained and the shunt system was removed on April 4. VPS was placed again on April 21 without further complications. She was symptom free for the next 7 years. Case 3 was a 57-year-old female who presented in a semicomatose state after falling from bed on May 5, 1995. CT scan showed left-sided acute subdural hematoma (ASDH) for which surgery was performed. Her neurological status improved postoperatively. She eventually developed hydrocephalus and left-sided subdural effusion for which right VPS and left subduroperitoneal shunt (SPS) surgery was performed on January 25, 1996. The peritoneal end of the tube of the SPS protruded out of the anus one and a half year after shunt placement. The entire SPS system was removed as there was no more collection in the subdural space. We reviewed the literature and discussed the pathophysiology involved in the development of intraabdominal complications following VPS.

[Experimental and clinical studies on liver tissue blood flow in obstructive jaundice].

To clarify some pathologic aspects of obstructive jaundice before and after bile duct drainage, changes in liver tissue blood flow were observed using an electrolytic historheometer, in combination with the FITC-dextran method, during experimental bile duct obstruction and after its elimination. Clinical investigations were based on histologic findings in liver tissue specimens collected by wedge biopsy at the time of laparotomy following bile duct drainage. Rats with bile duct obstruction showed significantly (P less than 0.01) lower values for liver tissue blood flow, with sinusoid dilation, in comparison to control rats, at 2 and 4 weeks following the initiation of experimental bile duct obstruction. Liver tissue blood flow disturbance subsided 3 days after eliminating the obstruction, at 2 weeks following its initiation, while no improvement occurred even following elimination of obstruction after 4 weeks. Clinically, in cases with a high degree of sinusoid dilation the effect of postoperative bile duct drainage was poor, with a high incidence of postoperative complication. These findings suggest that liver tissue blood flow disturbance might causatively affect the pre- and postoperative course of obstructive jaundice.