Potentiation of zinc stress caused by parasitic infection of snails

The purpose of this experiment was to determine the effects of parasitism (Schistosomatium douthitti Price and Trichobilharzia sp.) on the tolerance of snails Lymnaea stagnalis (L.) to acutely lethal concentrations of zinc. Significant reduction in tolerance occurred for snails with patent infections at 24 and 75 ppm of Zn⁺⁺. At two selected prepatent levels of parasite development, significant differences occurred at the higher concentration only.     

Role of isoprenoid compounds in plant adaptation to biogenic stress caused by parasitic nematodes

Parasitic nematodes are considered as a biogenic stress factor in plants. The effects of various plant isoprenoids, including mono-, sesqui-, di-, and triterpenoids, sterols, and steroid glycosides, on parasitic nematodes are reviewed. Certain isoprenoids can be placed in the class of natural plant adaptogens.     

Economic losses caused by foodborne parasitic diseases

Fragmentary data indicate that zoonotic parasites cause human illnesses with medical costs and productivity and disability losses totalling billions of dollars annually. Food is an important vehicle for some of these parasitic diseases. The cost to public health is not reflected in the priorities given to these parasitic diseases in either research or public health planning. In this article, Tanya Roberts, Darwin Murrell and Suzanne Marks discuss the cost of toxoplasmosis, taeniasis, cysticercosis, trichinellosis and other foodborne parasitic diseases.     

Oxidative stress and antioxidant defenses: a target for the treatment of diseases caused by parasitic protozoa

Parasitic protozoa cause several diseases, affecting hundreds of millions, particularly in underdeveloped countries. Although these organisms are eukaryotic cells, some of them present major differences with their mammalian host in selected metabolic pathways. These differences may be exploited as targets for developing better pharmacological agents for the treatment of specific parasitic diseases. This review describes some of the differences in terms of antioxidant defenses between these organisms and their mammalian host, which may provide useful targets for the treatment of these diseases. Some of the potential targets are: (i). iron metabolism in Plasmodium, (ii). the presence of a Fe-containing form of superoxide dismutase in trypanosomatids and malaria-causing parasites, (iii). the unique trypanothione-dependent antioxidant metabolism in trypanosomatids, (iv). the ascorbate peroxidase found in Trypanosoma cruzi and perhaps present in other trypanosomatids.     

Similarity of pathological alterations in insects during infection by microsporidia,other parasites and under different adverse environmental factors

Striking resemblance of pathological alterations in the development of insects caused by 1) infection with microsporidia, 2) infection with other parasites, and 3) variety of adverse environmental factors is discussed.     

Hypothesis for heritable, anti-viral immunity in crustaceans and insects

Correction to Flegel, TW: Hypothesis for heritable, anti-viral immunity in crustaceans and insects. Biology Direct 2009, 4:32.     

Hypothesis for heritable, anti-viral immunity in crustaceans and insects

Correction to Lindsay H, Yap VB, Ying H, Huttley GA: Pitfalls of the most commonly used models of context dependent substitution. Biology Direct 2008, 3:52     

Harmfulness of parasitic insects and acarines to mammals and birds

The paper summarizes the results of investigations on the harmfulness of the blood-sucking arthropods and ectoparasites to terrestrial vertebrates. Pathogenicity of parasitic arthropods strongly depends on the type of parasitism. Harmfulness to the hosts is analyzed separately in blood-sucking dipterans, ixodid ticks, gadflies, and both temporary (fleas and bugs) and permanent (biting lice, lice, acariform mites) ectoparasites. The pathogenicity of parasitic arthropods for the host organism is conditioned by the direct loss of blood and tissues, toxic effect of the arthropod’s saliva, and allergic reactions. Indirect injury from parasites is associated with deterioration of the host’s nutrition and loss of weight and viability. Pathogenicity for the host not resulting in its death is typical of parasitic arthropods, except for heavy attacks by blood-sucking Diptera which may lead to death of domesticated and wild animals. Most data on the pathogenicity of arthropods for vertebrates refer to domesticated animals. Annual losses to the world livestock breeding attributed to insects and acarines amount to several billion dollars. Direct evidence of ectoparasite pathogenicity to wild animals and effect on the host’s vital functions, reproduction, and population numbers in particular, is limited and unconvincing.     

Hypothesis: Environmental regulation of 5-hydroxymethylcytosine by oxidative stress

Many environmental toxins, such as heavy metals, air particles, and ozone, induce oxidative stress and decrease the levels of NADH and NADPH, cofactors that drive anabolic biochemical reactions and provide reducing capacity to combat oxidative stress. Recently, it was found that the Ten-eleven translocation (TET) protein family members, which oxidize 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) in the DNA, is activated under high oxygen conditions by alpha ketoglutarate (?-KG), a cofactor produced by aerobic metabolism in the citric acid cycle. TET, Jumonji-family histone demethylases, and prolyl hydroxylase, a repressor of HIF1a under high oxygen conditions, all require alpha ketoglutarate (a-KG) as cofactors for their activation. The impact of the HIF1a and TET proteins, which appear to have opposing functions, reaches several aspects of human life-including cell growth regulation, embryonic stem cell maintenance, cell differentiation, and tumorigenesis. The role of metabolism on regulating global DNA methylation and chromatin organization is recently demanding greater attention from the biomedical research community. This article will discuss the possible role of TET activation and the regulation of 5hmC and 5mC levels in response to environmental stress. We will also discuss how 5hmC and 5mC levels at the promoters of specific genes might be a useful biomarker for exposure to environmental toxins.     

Studies on parasitic castration: Aminopeptidase activity levels and protein concentrations in Ilyanassa obsoleta (mollusca) parasitized by larval trematodes

Specimens of the estuarine prosobranch Ilyanassa obsoleta collected in the vicinity of Charleston, South Carolina, during June, July, and August 1981, were found to be parasitized by larvae of the digeneans Cercaria dipterocerca, Himasthla quissetensis, Lepocreadium setiferoides, Microbilharzia variglandis, Microphalloides nassicola, Stephanostomum tenue, and Zoogonus lasius. The aminopeptidase activity levels and the total protein concentrations of the hemocytes and sera of these infected snails were determined. It was ascertained that snails parasitized by larvae of L. setiferoides had significantly higher levels of hemocytic aminopeptidase activity and hemocytic total protein concentrations than noninfected snails. Furthermore, snails parasitized by L. setiferoides larvae had significantly higher hemocytic levels of aminopeptidase activity than snails parasitized by larvae of S. tenue, Z. lasius, M. nassicola, and H. quissetensis.     

Time-dependent oxidative stress caused by benznidazole

Benznidazole (BZN) is a nitroimidazole derivative which has a notable trypanocide activity, and it is the only drug used in Brazil and Argentina for the treatment of Chagas' disease. The drug in current use is thought to act, at least in part, by inducing oxidative stress within the parasite. Imidazolic compounds are involved in the production of reactive oxygen species (ROS). In order to evaluate the effect of BZN on ROS production and on the antioxidant status of the host, male rats were treated for different periods of time (2, 4, 6, 10 and 30 days) with 40 mg BZN/kg body weight. After treatment, biomarkers of oxidative stress such as the activities of catalase (CAT), superoxide dismutase (SOD), glutathione-S-transferase (GST) and glutathione reductase (GR), and also thiobarbituric acid reactive species (TBARS), reduced glutathione (GSH), total glutathione (TG) and oxidized glutathione (GSSG) concentrations, were measured in crude hepatic homogenates. Our results revealed that BZN is able to cause tissue damage as shown by increased TBARS content, inhibition of some antioxidants and induction of other antioxidants in a concentration- and time-dependent manner. The tissue damage measured as TBARS increased up to the 10th day of treatment. GST activity was inhibited during the BZN treatment. On the other hand, CAT and GR showed similar increased activities at the beginning, followed by decreased activities at the end of the treatment. After 30 days of treatment, GR activity remained low while CAT activity was high, compared to controls. The SOD activities remained unchanged throughout the experimental period. GSH showed lower values at the beginning of BZN treatment but the hepatic concentrations were enhanced at the end of the experimental period. Total glutathione showed a similar profile, and oxidized glutathione showed higher values in rats treated with BZN. In conclusion, these results indicate that, at therapeutic doses, BZN treatment elicits an oxidative stress in rat hepatocytes.     

Time-dependent oxidative stress caused by benznidazole

Abstract

Benznidazole (BZN) is a nitroimidazole derivative which has a notable trypanocide activity, and it is the only drug used in Brazil and Argentina for the treatment of Chagas' disease. The drug in current use is thought to act, at least in part, by inducing oxidative stress within the parasite. Imidazolic compounds are involved in the production of reactive oxygen species (ROS). In order to evaluate the effect of BZN on ROS production and on the antioxidant status of the host, male rats were treated for different periods of time (2, 4, 6, 10 and 30 days) with 40 mg BZN/kg body weight. After treatment, biomarkers of oxidative stress such as the activities of catalase (CAT), superoxide dismutase (SOD), glutathione-S-transferase (GST) and glutathione reductase (GR), and also thiobarbituric acid reactive species (TBARS), reduced glutathione (GSH), total glutathione (TG) and oxidized glutathione (GSSG) concentrations, were measured in crude hepatic homogenates. Our results revealed that BZN is able to cause tissue damage as shown by increased TBARS content, inhibition of some antioxidants and induction of other antioxidants in a concentration- and time-dependent manner. The tissue damage measured as TBARS increased up to the 10th day of treatment. GST activity was inhibited during the BZN treatment. On the other hand, CAT and GR showed similar increased activities at the beginning, followed by decreased activities at the end of the treatment. After 30 days of treatment, GR activity remained low while CAT activity was high, compared to controls. The SOD activities remained unchanged throughout the experimental period. GSH showed lower values at the beginning of BZN treatment but the hepatic concentrations were enhanced at the end of the experimental period. Total glutathione showed a similar profile, and oxidized glutathione showed higher values in rats treated with BZN. In conclusion, these results indicate that, at therapeutic doses, BZN treatment elicits an oxidative stress in rat hepatocytes.     

Histopathology in hosts parasitized by Sarcoptes scabiei

Histopathologic evaluation of nondermal tissue in rabbits infested with Sarcoptes scabiei var. canis was investigated. Severe infestation resulted in deviant serological and serum biochemical values. Histological study revealed structural changes in the tissues of specific organs. The most prominent histological finding was amyloidosis in the liver, glomerulus of the kidney, red pulp of the spleen, intestines, and tongue. Hosts treated for infestation exhibited no abnormal organ histology.