Adherence to antiretroviral therapy (ART) plays an important role in the treatment outcomes of human immunodeficiency virus (HIV) infection. Poor adherence would result in failure to prevent viral replication as well as an increased risk of developing drug resistance. Adherence to a life long treatment such as antiretroviral therapy is usually a complicated issue that requires careful and continuous collaboration of patient, family and healthcare provider. The objective of this study was to assess adherence to antiretroviral therapy and its associated factors among people living with HIV. This is a health facility-based cross sectional study conducted among adults’ people living with HIV in Omdurman HIV/AIDS centre, Sudan. Data was collected through direct interview using semi-structured questionnaire. There were only 144/846 (17.02%) who adhered to antiretroviral therapy as prescribed by their doctors. The remaining 51.18% were taking the therapy but not regularly, 31.21% were taking it but currently not and 0.59% stated that they have never taken any antiretroviral therapy. Factors associated with poor adherence that have been identified include female gender (Adj. OR = 3.46 (95%CI: 1.46–8.21), P = 0.005), younger age (Adj. OR = 1.14 (95%CI: 1.02–1.28), P = 0.022), being unemployed (Adj. OR = 5.94 (95%CI: 1.51–23.40), P = 0.011), those who were divorced, separated or widowed (Adj. OR = 11.35 (95%CI: 1.74–73.96), P = 0.011) and respondents who perceived that their health status is poor (Adj. OR = 5.21 (95%CI: 1.44–18.81), P = 0.012) or very poor (Adj. OR = 4.04 (95%CI: 1.27–12.81), P = 0.018). Educational level and social support against HIV-related stigma and discrimination were not significantly associated with adherence. Adherence to antiretroviral therapy among the respondents is very poor. Urgent interventions based on modifiable factors and mainly targeting females and younger age group are needed to improve adherence to antiretroviral therapy among people living with HIV.
HIV ; Antiretroviral Therapy, Highly Active ; Therapeutics ; Adult

OBJECTIVETo determine the efficiency of selenium and/or vitamin E to alleviate lung oxidative damage induced by dimethoate, an organophosphorus compound.

METHODSAdult Wistar rats were exposed during 30 days either to dimethoate (0.2 g/L of drinking water), dimethoate+selenium (0.5 mg/kg of diet), dimethoate+vitamin E (100 mg/kg of diet), or dimethoate+selenium+vitamin E.

RESULTSExposure to dimethoate caused oxidative stress in lung evidenced by an increase of malondialdehyde, protein carbonyl groups and advanced oxidation protein products. An increase in glutathione peroxidase, superoxide dismutase, catalase and a decrease in acetylcholinesterase and butyrylcholinesterase activities, glutathione, non-protein thiols and vitamins C levels were observed. Histopathological changes in lung tissue were noted as emphysema, hemorrhages and hemosiderin deposits. Co-administration of selenium or vitamin E to the diet of dimethoate treated rats ameliorated the biochemical parameters as well as histological impairments. The joint effect of these elements was more powerful in antagonizing dimethoate-induced lung oxidative damage.

CONCLUSIONWe concluded that selenium and vitamin E ameliorated the toxic effects of this pesticide in lung tissue suggesting their role as potential antioxidants.

Acetylcholinesterase ; metabolism ; Animals ; Antioxidants ; administration & dosage ; pharmacology ; Ascorbic Acid ; metabolism ; Biomarkers ; Butyrylcholinesterase ; metabolism ; Dimethoate ; adverse effects ; Glutathione ; metabolism ; Lipid Peroxidation ; drug effects ; Lung Diseases ; diagnosis ; prevention & control ; Oxidative Stress ; Rats ; Rats, Wistar ; Selenium ; administration & dosage ; pharmacology ; Vitamin E ; administration & dosage ; pharmacology

OBJECTIVEEmbryonic movements (EM) and angiogenesis pathways are evolutionarily conserved mechanisms which are essential for proper embryonic development. Deviations in these processes by exposure to cigarette smoke condensate (CSC) may cause vascular and morphogenetic disorders.

METHODSUsing chicken and mouse embryos, we have demonstrated the in vivo effects of CSC on EM, vascular development, and organogenesis.

RESULTSExamination of the CSC exposed chicken embryos revealed a significant reduction in EM, stunted growth, deviated pattern of blood vessels, hemorrhages, and localized necrosis. Likewise, mouse embryos that were exposed to CSC at E8.5 and E9.5 died between E11.5 and E12.5, respectively. These mouse embryos showed defects in morphogenesis and remodeling of the embryonic vasculature, while littermate controls showed normal development.

CONCLUSIONSCigarette smoking during pregnancy is fatal for growing embryos. CSC may induce the remodeling of embryonic vasculature, leading to various pathologies.

Analysis of Variance ; Animals ; Chick Embryo ; Embryonic Development ; drug effects ; Female ; Maternal Exposure ; adverse effects ; Mice ; Mice, Inbred C57BL ; Movement ; drug effects ; Organogenesis ; drug effects ; Pregnancy ; Smoke ; adverse effects ; Tobacco ; Vascular Malformations ; chemically induced

Objective: This research was performed to evaluate the effect of tebuconazole (TBZ) on reproductive organs of male rats and to assess the protective role of combined essential trace elements in alleviating the detrimental effect of TBZ on male reproductive function. Methods: For this purpose, 48 rats were exposed to 100 mg/kg TBZ, TBZ supplemented with zinc (Zn), selenium (Se), copper (Cu), and iron (Fe), TBZ + (Se + Zn); TBZ + Cu; or TBZ + Fe. The experiment was conducted for 30 consecutive days. Results: TBZ caused a significant perturbation in mineral levels and reduction in reproductive organs weights, plasma testosterone level, and testicular antioxidant enzyme activities. The TBZ-treated group also showed a significant increase in sperm abnormalities (count, motility, and viability percent), plasma follicle-stimulating hormone and luteinizing hormone concentrations, lipid peroxidation, protein oxidation, and severe DNA degradation in comparison with the controls. Histopathologically, TBZ caused testis impairments. Conversely, treatment with trace elements, in combination or alone, improved the reproductive organ weights, sperm characteristics, TBZ-induced toxicity, and histopathological modifications in testis. Conclusion TBZ exerts significant harmful effects on male reproductive system. The concurrent administration of trace elements reduces testis dysfunction, fertility, and toxicity induced by TBZ.
Animal Feed/analysis* ; Animals ; Antioxidants/metabolism* ; Diet ; Dietary Supplements/analysis* ; Fungicides, Industrial/adverse effects* ; Male ; Minerals/metabolism* ; Mutagenicity Tests ; Rats ; Rats, Wistar ; Spermatozoa/physiology* ; Testis/physiology* ; Trace Elements/metabolism* ; Triazoles/adverse effects*

OBJECTIVE: The current study aimed to elucidate the effect of vanillin on behavioral changes, oxidative stress, and histopathological changes induced by potassium bromate (KBrO3), an environmental pollutant, in the cerebellum of adult mice. METHODS: The animals were divided into four groups: group 1 served as a control, group 2 received KBrO3, group 3 received KBrO3 and vanillin, and group 4 received only vanillin. We then measured behavioral changes, oxidative stress, and molecular and histological changes in the cerebellum. RESULTS: We observed significant behavioral changes in KBrO3-exposed mice. When investigating redox homeostasis in the cerebellum, we found that mice treated with KBrO3 had increased lipid peroxidation and protein oxidation in the cerebellum. These effects were accompanied by decreased Na+-K+ and Mg2+ ATPase activity and antioxidant enzyme gene expression when compared to the control group. Additionally, there was a significant increase in cytokine gene expression in KBrO3-treated mice. Microscopy revealed that KBrO3 intoxication resulted in numerous degenerative changes in the cerebellum that were substantially ameliorated by vanillin supplementation. Co-administration of vanillin blocked the biochemical and molecular anomalies induced by KBrO3. CONCLUSION Our results demonstrate that vanillin is a potential therapeutic agent for oxidative stress associated with neurodegenerative diseases.
Animals ; Antioxidants ; metabolism ; Behavior, Animal ; drug effects ; Benzaldehydes ; pharmacology ; Bromates ; toxicity ; Cerebellum ; drug effects ; metabolism ; pathology ; Cytokines ; genetics ; metabolism ; Environmental Pollutants ; toxicity ; Gene Expression ; drug effects ; Lipid Peroxidation ; drug effects ; Mice ; Oxidative Stress ; drug effects ; Rotarod Performance Test