Insight into hematological parameters of petrol station workers.

OBJECTIVE: Benzene is one of the major carcinogenic factors that can affect liver, kidneys, and lungs. Chronic inhalation of benzene vapor by petrol stations workers has been shown to have an impact on hematological parameters; thus, the present study aimed to investigate the effect of benzene exposure on petrol station workers. SUBJECTS AND METHODS: The study involved 99 participants, 50 of whom have been exposed to benzene and 49 of whom have not (control). A 5 ml blood sample in an ethylenediaminetetraacetic acid (EDTA) anticoagulant tube was collected from each subject, and a complete blood count test was used to test hematological parameters. RESULTS: The current study showed a significant decrease in red blood cells, packed cell volume, and hemoglobin in the exposed group compared to the control group. However, the amount of white blood cells was significantly increased (p < 0.0001) in the exposed group compared to the control group. Notably, there was no significant difference in platelet counts between the two groups. In terms of exposure time, subjects who have been exposed to benzene for more than a year and fewer than 10 years showed a significant decrease (p < 0.05) in RBCs indices and a significant increase (p < 0.0001) in WBCs compared to those in the control group CONCLUSIONS: Thus, the findings indicated that significant differences in hematological parameters were found in workers who were exposed to benzene compared to those who had not been exposed.

Chemokines are produced in the brain early during the course of experimental African trypanosomiasis.

African trypanosomiasis is characterized by progressive central nervous system (CNS) involvement. Using single and double immunohistochemistry, we evaluated the induction of alpha- and beta-chemokines in brains of Sprague-Dawley rats infected with Trypanosoma brucei brucei (T. b. brucei) and identified their cellular source. The results showed high production of MIP-2, RANTES and MIP-1alpha and to a lower extend MCP-1 in infected animals compared to controls. MIP-2, RANTES and MIP-1alpha were produced early by astrocytes and microglia and later by macrophages and T-cells. These findings suggest that chemokines may contribute to the immunopathogenesis that occurs in the CNS early during infections.

Trypanosoma brucei brucei induces interferon-gamma expression in rat dorsal root ganglia cells via a tyrosine kinase-dependent pathway.

Dorsal root ganglia (DRG) were shown to express neuronal interferon (IFN)-gamma, which supports Trypanosoma brucei brucei growth. The ability of a trypanosome-derived factor (TLTF) to activate DRG to neuronal IFN-gamma secretion was investigated, together with the signaling pathway that might be involved during this process. Immunohistochemical staining revealed expression of neuronal IFN-gamma on stimulation with TLTF, which was blocked with the tyrosine protein-kinase inhibitor, tyrphostin A47. Western blot was used to analyze DRG lysates prepared at different time points after stimulation with TLTF. A tyrosine-phosphorylated protein induced at 15 min was seen as a band of 120-150 kDa, followed by a decrease to control levels after 30 min. A47 greatly suppressed the TLTF-induced tyrosine protein kinase activity. In addition, evidence suggesting that the transcription factor STAT-1 may play a key role in the TLTF signaling pathway was provided by the blocking effects of A47 on STAT-1 translocation to the nucleus.

Cytokines and anti-cytokine autoantibodies during experimental african trypanosomiasis in mice with disrupted interferon-gamma and interferon-gamma receptor genes.

We studied cytokines and anti-cytokine autoantibodies (Aabs) during T.b.brucei infections in IFN-gamma-/-, IFN-gammaR-/- and wild-type mice. Increased serum levels of IFN-gamma, TNF-gamma and IL-4 with decreased Aabs to these cytokines were recorded early during infections in all mice (except IFN-gamma in IFN-gamma-/- mice). Later, these responses were reversed, and surprisingly Aabs reacting to IFN-gamma in the IFN-gamma -/- mice were detected. To examine the possibility that an IFN-ç immunoreactive molecule might be expressed due to infections and upon gene deletion, anti-IFN-gamma antibody was inoculated and resulted in abrogation of such Aabs. The scenario was different for IL-10 and TGF- since IFN-gammaR-/- and wild-type mice showed low cytokines and high Aabs early during infections, but later high cytokines and low Aabs were registered. Interestingly, IFN-gamma-/- mice exhibited reversed levels of both IL-10 and TGF-beta, and also of their Aabs. Fab fragments of purified serum immunoglobulins showed binding and neutralizing effects in biological assays. Pre-absorption of the Fab fragments with a cytokine inhibited the binding and neutralization effects of this cytokine, but not of other cytokines. These results highlight an important role for autoimmunity in cytokine regulation, and that genomic deletion of IFN-gamma modulates cytokines and their Aab responses in experimental African trypanosomiasis.

Altered neuronal activity rhythm and glutamate receptor expression in the suprachiasmatic nuclei of Trypanosoma brucei-infected rats.

The parasites Trypanosoma brucei cause African trypanosomiasis (sleeping sickness), a severe neuropsychiatric disease with marked disturbances of sleep-wake alternation. The sites of brain lesions are not well characterized. The present experimental investigation is focused on the hypothalamic suprachiasmatic nuclei, which play a role of a biological clock entraining endogenous rhythms in the mammalian brain. The electrophysiological properties of these neurons were analyzed in slice preparations from trypanosome-infected rats. The neuronal spontaneous activity, which shows a circadian oscillation, was markedly altered in the infected animals, displaying a reduced firing rate and phase advance of its circadian peak. The direct retinal fibers, which play a pivotal role in entrainment of the circadian pacemaker, displayed a normal density and distribution in the suprachiasmatic nuclei of infected animals after intraocular tracer injections in vivo. At the postsynaptic level, immunohistochemistry and Western blotting revealed in the suprachiasmatic nuclei of infected rats a selective decrease of the expression of glutamate AMPA GluR2/3 and NMDAR1 receptor subunits that gate retinal afferents. These data disclose an impairment of the neuronal functions in the biological clock in African trypanosomiasis, and may serve to unravel functional and molecular mechanisms behind endogenous rhythm disturbances.