Infectious diseases caused by parasites are a major threat for the entire mankind, especially in the tropics. More than 1 billion people world-wide are directly exposed to tropical parasites such as the causative agents of trypanosomiasis, leishmaniasis, schistosomiasis, lymphatic filariasis and onchocerciasis, which represent a major health problem, particularly in impecunious areas. Unlike most antibiotics, there is no “general” antiparasitic drug available. Here, the selection of antiparasitic drugs varies between different organisms. Some of the currently available drugs are chemically de novo synthesized, however, the majority of drugs are derived from natural sources such as plants which have subsequently been chemically modified to warrant higher potency against these human pathogens. In this review article we will provide an overview of the current status of plant derived pharmaceuticals and their chemical modifications to target parasite-specific peculiarities in order to interfere with their proliferation in the human host.

To elucidate the function of Omega class glutathione transferases (GSTs) (EC 2.5.1.18) in multicellular organisms, the GSTO‐1 from Caenorhabditis elegans (GSTO‐1; C29E4.7) was investigated. Disc diffusion assays using Escherichia coli overexpressing GSTO‐1 provided a test of resistance to long‐term exposure under oxidative stress. After affinity purification, the recombinant GSTO‐1 had minimal catalytic activity toward classic GST substrates but displayed significant thiol oxidoreductase and dehydroascorbate reductase activity. Microinjection of the GSTO‐1 ‐promoter green fluorescent protein construct and immunolocalization by electron microscopy localized the protein exclusively in the intestine of all postembryonic stages of C. elegans. Deletion analysis identified an ~300‐nucleotide sequence upstream of the ATG start site necessary for GSTO‐1 expression. Site‐specific mutagenesis of a GATA transcription factor binding motif in the minimal promoter led to the loss of reporter expression. Similarly, RNA interference (RNAi) of Elt‐2 indicated the involvement of this gut‐specific transcription factor in GSTO‐1 expression. Transcriptional up‐regulation under stress conditions of GSTO‐1 was confirmed by analyzing promoter‐reporter constructs in transgenic C. elegans strains. To investigate the function of GSTO‐1 in vivo , transgenic animals overexpressing GSTO‐1 were generated exhibiting an increased resistance to juglone‐, paraquat‐, and cumene hydroperoxide‐induced oxidative stress. Specific silencing of the GSTO‐1 by RNAi created worms with an increased sensitivity to several prooxidants, arsenite, and heat shock. We conclude that the stress‐responsive GSTO‐1 plays a key role in counteracting environmental stress.—Burmeister, C., Lüersen, K., Heinick, A., Hussein, A., Domagalski, M., Walter, R. D., Liebau, E. Oxidative stress in Caenorhabditis elegans : protective effects of the Omega class glutathione transferase ( GSTO‐1 ). FASEB J. 22, 343–354 (2008)

A review of knowledge on plant extracts with known polyphenolic composition and of defined polyphenols against intestinal nematodes, focussing on polyphenols mainly from condensed and hydrolysable tannins, flavonoids and phenylpropanoids and their diverse biological activity against different helminths including the underlying mechanisms.

The ubiquitin-fold modifier 1 (Ufm1) is a posttranslational modifier that belongs to the ubiquitin-like protein (UBL) family. Ufm1 is present in nearly all eukaryotic organisms, with the exception of fungi. It resembles ubiquitin in its ability to be ligated to other proteins, as well as in the mechanism of ligation. While the Ufm1 cascade has been implicated in endoplasmic reticulum functions and cell cycle control, its biological role still remains poorly understood. In this short review, we summarize the current state of Ufm1 research and its potential role in human diseases, like diabetes, ischemic heart disease and cancer.

Apicomplexan parasites cause infectious diseases that are either a severe public health problem or an economic burden. In this paper we will shed light on how oxidative stress can influence the host-pathogen relationship by focusing on three major diseases: babesiosis, coccidiosis, and toxoplasmosis.