In Vitro Induced Resistance of Fusarium Wilt Disease (Fusarium oxysporum f.sp. cepae) by Salicylic Acid in Shallot CV ‘Bima Brebes’

Fusarium wilt caused by Fusarium oxysporum f.sp.cepae (Foc) is one of the most important diseases of onion in Indonesia. Induced resistance was one of the effective techniques to acquire resistance to fusarium wilt in shallot. Salicylic acid (SA) had been inferred to be in endogenous signal in the systemic acquired resistance response of plants. This research aimed to study the effect of exogenously added SA to resistance in shallot callus cv ‘Bima Brebes’ to fusarium wilt disease in vitro; and to determine the effective concentration of SA to induce resistance. A group of shallot callus was grown in MS medium containing varying SA concentration (0, 15, 20 and 25 ppm) in vitro for 2 weeks. Then, the callus were treated with toxin of Fusarium oxysporum, namely fusaric acid, to have observe the resistance response. In vitro selection was done twice in different fusaric acid concentration. Application of exogenous SA at all concentration did not suppres time of appearance of disease symptom yet. Toxic symptom in the callus was shown by the browning or blackening (off) of callus. Salicylic acid at concentration of 20 ppm effectively reduced the toxic symptom up to 16.66% and supported callus regeneration better than the concentration of 15 ppm and 25 ppm. The number of resistant callus regenerated was 66.67% at pretreatment of 20 ppm of SA.

A SUBCHRONIC TOXICITY TEST OF ETHANOL EXTRACT FROM TUNJUK LANGIT RHIZOME (HELMINTHOSTACHYS ZEYLANICA) ON ALBINO RATS, RATTUS NOVERTICUS (WISTAR STRAIN)

Objective: Traditionally, Tunjuk langit (Helmynthostachis zaylanica) rhizome has been used as anticancer and anti-inflammation drugs; however, it may have toxic effects on major organs for a long-term continuously consecutive consumption. Therefore, this study was carried out to test sub- chronic toxicity of the ethanol extract of the rhizome on Albino rats, Rattus noverticus (Wistar strain). Methods: A total of 100 male and female rats were divided into five groups. Groups I, II, III, and IV were orally administered with ethanol extracts of 68, 136, 272, and 554 mg/kg body weight (BW), respectively. Meanwhile, Group V used as a control was no treatment with the extract. A toxic symptom has been observed by analyzing several parameters, namely BW, hematologic and biochemical properties, macroscopic organs, and relative organ weight.Results: In general, the results show that there is no any toxic symptom and statistically insignificant differences in these parameters between treated and control groups. Conclusion: We conclude that the ethanol extract of Tunjuk Langit rhizome does not have effects of subchronic toxicity.Keywords: Tunjuk langit rhizome, Ethanol extract, Subchronic toxicity.

Surfactant toxicity in a case of (4-chloro-2-methylphenoxy) acetic acid herbicide intoxication

Objective: Self-poisoning with (4-chloro-2-methylphenoxy) acetic acid (MCPA) is a common reason for presentation to hospitals, especially in some Asian countries. We encountered a case of a 76-year-old woman who experienced unconsciousness, shock and respiratory failure after ingesting 100 mL MCPA herbicide. We determined whether the surfactant in the formulation was the chemical responsible for the toxic symptom in this patient. Design: 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) cell viability and lactate dehydrogenase (LDH) cytotoxicity assays were performed on human brain neuroblastoma SK-N-SH cells. The expressions of 84 genes in 9 categories that are implicated in cellular damage pathways were quantified using an RT2 Profiler™ PCR array on a human neuronal cell line challenged with polyoxyethylene tridecyl ether (PTE). Setting: Pesticide intoxication institute in university hospital. Interventions: Extracorporeal elimination with intravenous lipid emulsion. Measurements: Cell viability and gene expression. Main Results: In the MTT assay, MCPA only minimally decreased cell viability even at concentrations as high as 1 mM. Cells treated with 1-methoxy-2-propanol, dimethylamine and polypropylene glycol exhibited minimal decreases in viability, whilst the viability of cells challenged with PTE decreased dramatically; only 15.5% of cells survived after exposure to 1 µM PTE. Similarly, the results of the LDH cytotoxicity assay showed that MCPA had very low cytotoxicity, whilst cells treated with PTE showed incomparably higher LDH levels ( p < 0.0001). PTE up-regulated the expressions of genes implicated in various cell damage pathways, particularly genes involved in the inflammatory pathway. Conclusions: The surfactant PTE was likely the chemical responsible for the toxic symptom in our patient.