Altertoxin I

Alternariacauses pathogenic disease on various economically important crops having saprophytic to endophytic lifecycle. Pathogenic fungi ofAlternariaspecies produce many primary and secondary metabolites (SMs).Alternariaspecies produce more than 70 mycotoxins. Several species ofAlternariaproduce various phytotoxins that are host-specific (HSTs) and non-host-specific (nHSTs). These toxins have various negative impacts on cell organelles including chloroplast, mitochondria, plasma membrane, nucleus, Golgi bodies, etc. Non-host-specific toxins such as tentoxin (TEN), Alternaric acid, alternariol (AOH), alternariol 9-monomethyl ether (AME), brefeldin A (dehydro-), Alternuene (ALT), Altertoxin-I, Altertoxin-II, Altertoxin-III, zinniol, tenuazonic acid (TeA), curvularin and alterotoxin (ATX) I, II, III are known toxins produced byAlternariaspecies. In other hand,Alternariaspecies produce numerous HSTs such as AK-, AF-, ACT-, AM-, AAL- and ACR-toxin, maculosin, destruxin A, B, etc. are host-specific and classified into different family groups. These mycotoxins are low molecular weight secondary metabolites with various chemical structures. All the HSTs have different mode of actions, biochemical reactions, and signaling mechanisms to causes diseases in the host plants. These HSTs have devastating effects on host plant tissues by affecting biochemical and genetic modifications. Host-specific mycotoxins such as AK-toxin, AF-toxin, and AC-toxin have the devastating effect on plants which causes DNA breakage, cytotoxic, apoptotic cell death, interrupting plant physiology by mitochondrial oxidative phosphorylation and affect membrane permeability. This article will elucidate an understanding of the disease mechanism caused by severalAlternariaHSTs on host plants and also the pathways of the toxins and how they caused disease in plants.

Alternaria alternata is a common fungal parasite on fruits and other plants and produces a number of mycotoxins, including alternariol (3,7,9-trihydroxy-1-methyl-6H-dibenzo [b,d]pyran-6-one), alternariol monomethyl ether (3,7-dihydroxy-9-methoxy-1-methyl-6H-dibenzo[b,d]pyran-6-one), and the mutagen altertoxin I {[1S-(1α,12aβ,12bα)] 1,2,11,12,12a, 12b-hexahydro-1,4,9,12a-tetrahydroxy-3,10-perylenedione}. Alternariol and alternariol monomethyl ether have previously been detected in some samples of fruit beverages. Stability studies of these toxins as well as altertoxin I added to fruit juices and wine (10-100 ng/mL) were carried out. To include altertoxin I in the analysis, cleanup with a polymer-based Varian Abselut solid phase extraction column was used, as recoveries from C-18 columns were low. The stabilities of alternariol and alternariol monomethyl ether in a low acid apple juice containing no declared vitamin C were compared with those in the same juice containing added vitamin C (60 mg/175 ml); there were no apparent losses at room temperature over 20 days or at 80°C after 20 min. in either juice. Altertoxin I was moderately stable in pH 3 buffer (75% remaining after a two week period). Furthermore, altertoxin I was stable or moderately stable in three brands of apple juice tested over 1-27 day periods and in a sample of red grape juice over 7 days. It is concluded that altertoxin I is sufficiently stable to be found in fruit juices and should be included in methods for alternariol and alternariol monomethyl ether.

Purified Alternaria alternata altertoxins I, II, and III were evaluated for comparative cytotoxicity and ability to inhibit gap junction communication in the Chinese hamster lung metabolic cooperation assay. The noncytotoxic test range for each altertoxin was determined for the metabolic communication assays: altertoxin I, 1, 2, 3, 4, 5 micrograms/ml; altertoxin II, 0.02, 0.008, 0.006, 0.004, 0.002, 0.0008 micrograms/ml; and altertoxin III, 0.2, 0.1, 0.08, 0.06, 0.04 micrograms/ml. Altertoxin II was the most cytoxic in the V79 system, followed by altertoxins III and I. The last cytotoxic of the three, altertoxin I, weakly disrupted metabolic communication at two concentrations (4 and 5 micrograms/ml). Altertoxins III and II did not significantly inhibit gap junction communication more than the weak tumor promoter 4-O-methyl ether tetradecanoylphorbol 13-acetate.