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Pyrethroids are widely used insecticides of low acute toxicity in mammals but the consequences of long-term exposure are of concern. Their insecticidal action is related to neurotoxicity and, in addition, there are indications of mammalian immuno-toxicity. In this work the effect of 60 days permethrin (150 mg kg(-1) body weight/day) exposure on two types of leukocytes (monocytes and lymphocytes) in adolescent rats was investigated. In particular, the monocyte respiratory burst response was first investigated, followed by studies on the degree and type of lymphocyte DNA damage induced by permethrin at this stage of life. Permethrin treatment reduces the monocyte respiratory burst response to phorbol myristate acetate, thereby decreasing superoxide anion (65%) and hydrogen peroxide (37%) production. Moreover an increase [correction made here after initial online publication] in monocyte plasma membrane fluidity in the hydrophilic-hydrophobic interface of the lipid bilayer was measured. Data obtained from the comet assay show that permethrin induces lymphocyte DNA lesions at both formamido pyrimidine glycosylase (Fpg) and endonuclease III (Endo III) sites in adolescent rats. Our results indicate the key role of permethrin in oxidative stress whose consequences lead to biochemical and functional changes. The reduced phagocyte respiratory burst induced by permethrin treatment and the type of DNA damage measured could represent new relevant aspects of pyrethroid toxicity which should be considered for human health.

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A series of multifunctional codrugs (1-6) were synthesized to overcome the pro-oxidant effect associated with L-dopa (LD) therapy. Target compounds release LD and dopamine (DA) in human plasma after enzymatic hydrolysis, displaying an antioxidant effect superior to that of N-acetylcysteine (NAC). After intracerebroventricular injection of codrug 4, the levels of DA in the striatum were higher than those in LD-treated groups, indicating that this compound has a longer half-life in brain than LD.