Genetic diversity and population structure of Striga hermonthica populations from Kenya and Nigeria

Article purchasedStriga hermonthica is a parasitic weed that poses a serious threat to the production of economically important cereals in sub-Saharan Africa. The existence of genetic diversity within and between S. hermonthica populations presents a challenge to the successful development and deployment of effective control technologies against this parasitic weed. Understanding the extent of diversity between S. hermonthica populations will facilitate the design and deployment of effective control technologies against the parasite. In the present study, S. hermonthica plants collected from different locations and host crops in Kenya and Nigeria were genotyped using single nucleotide polymorphisms. Statistically significant genetic differentiation (FST = 0.15, P = 0.001) was uncovered between populations collected from the two countries. Also, the populations collected in Nigeria formed three distinct subgroups. Unique loci undergoing selection were observed between the Kenyan and Nigerian populations and among the three subgroups found in Nigeria. Striga hermonthica populations parasitising rice in Kenya appeared to be genetically distinct from those parasitising maize and sorghum. The presence of distinct populations in East and West Africa and in different regions in Nigeria highlights the importance of developing and testing Striga control technologies in multiple locations, including locations representing the geographic regions in Nigeria where genetically distinct subpopulations of the parasite were found. Efforts should also be made to develop relevant control technologies for areas infested with ‘rice-specific’ Striga spp. populations in Kenya

Modulation of the oxidative stress in malaria infection by clotrimazole

Antimycotic clotrimazole (CTZ) has demonstrated remarkable activity against Plasmodium falciparum in vitro and in vivo. Hemoglobin degradation by Plasmodium parasites makes amino acids available for protein synthesis, inducing oxidative stress in infected cells and producing free heme. These events represent biochemical targets for potential antimalarials. In this study, we have tested the ability of CTZ to modify the oxidative status in Plasmodium berghei-infected erythrocytes. After hemolysis, activities of superoxide dismutase (SOD), catalase (CAT), glutathione cycle and NADPH+H+-producing dehydrogenases were investigated using UV-visible spectrophotometry. Thiobarbituric acid reactive substances (TBARS) were evaluated as a marker of lipid damage. Results showed that CTZ significantly decreased the overall activity of 6-phosphagluconate dehydrogenase (6PGD) compared to infected and non-treated cells; consequently, the glutathione cycle was inhibited, leaving the parasite vulnerable to the oxidative stress originating from hemoglobin degradation. As a compensatory response, CTZ prevented some loss of SOD and CAT activities in infected cells. The infection triggered lipid peroxidation in erythrocytes, which was decreased by CTZ. These results suggest the presence of a redox unbalance in cells treated with CTZ, discussing a possible effect of this compound disturbing the oxidative status in a Plasmodium berghei-infection.O antifúngico clotrimazol (CTZ) tem demonstrado notável atividade contra Plasmodium falciparum. A degradação da hemoglobina por Plasmodium para a obtenção dos aminoácidos necessários à síntese protéica induz estresse oxidativo em eritrócitos devido à liberação de hemos oxidantes. Estes eventos representam alvos bioquímicos para a produção de antimaláricos potenciais. Neste estudo, testamos a capacidade do CTZ para modificar o estado oxidativo em eritrócitos infectados com Plasmodium berghei. Depois da hemólise, as atividades da superóxido dismutase (SOD), catalase (CAT), desidrogenases produtoras de NADPH+H+ e do ciclo de glutationa (GSH) foram investigados. A produção das espécies reativas ao ácido tiobarbitúrico (TBARS) foi avaliada como marcador de dano lipídico. Os resultados mostraram que o CTZ diminuiu a atividade da 6-fosfogliconato desidrogenase (6PGD), em comparação com eritrócitos infectados e não tratados. Consequentemente, o ciclo da GSH foi inibido, tornando os parasitas vulneráveis ao estresse oxidativo resultante da degradação da hemoglobina. Como resposta compensatória, CTZ impediu a perda de atividade da SOD e CAT nas células infectadas. A infecção induz peroxidação lipídica nos eritrócitos, sendo esta diminuída pelo CTZ. Estes resultados sugerem a existência de desequilíbrio redox nas células tratadas com CTZ, interferindo, assim, com o estado oxidativo verificado durante a infecção malárica

Direct effect of p,p'- DDT on mice liver

ABSTRACT Contact with the pesticide dichlorodiphenyltrichloroethane (p,p′-DDT) can be the cause of various harmful effects in humans, wildlife, and the environment. This pesticide is known to be persistent, lipophilic, resistant to degradation, and bioaccumulive in the environment and to be slowly released into bloodstream. Growing evidence shows that exposure to DDT is linked to type 2 diabetes mellitus. Individuals exposed to elevated levels of DDT and its metabolite have an increased prevalence of diabetes and insulin resistance. To evaluate these possible relationships, experiments were performed on eight-week-old female mice, divided into three groups (n = 10 per group): Group 1 received a vehicle-control intraperitoneal (i.p.) injection of sesame oil; Groups 2 and 3 received an i.p. dose of 50 and 100 µg/g p,p′-DDT respectively, dissolved in sesame oil. All groups were treated once daily for four days. Real-time PCR analysis of several genes was undertaken. Additionally, biochemical parameters and histopathological changes were measured. NQO1, HMOX1, NR1I3 and NR3C1 were up-regulated in DDT-exposed animals compared to the vehicle control group, while only SREBP1 was down-regulated in the 100 µg/g group. MTTP and FABP5, not previously reported for DDT exposure, but involved in regulation of fatty acid fluxes, could also function as biomarkers cross-talking between these signaling pathways. These results suggest that beyond epidemiological data, there is increasing molecular evidence that DDT may mimic different processes involved in diabetes and insulin resistance pathways

Sub-acute toxicity study of ethylene glycol monomethyl ether on the antioxidant defense system of the testes and epididymes of wistar rats

Summary: Ethylene glycol monomethyl ether is a toxicant with wide industrial applications. This study is aimed at investigating its effect on the antioxidant system of the reproductive organs of male rats. Fifty male Wistar rats were distributed into five groups. Group I received distilled water, Groups II-V received EGME at 100, 200, 300 and 400 mg/kg body weight respectively. All administrations were done orally for fourteen days and the weight was monitored weekly. On day fifteen, the animals were sacrificed and reproductive organs were collected and weighed. The testes and epididymes were processed for the biochemical estimations, histopathology and spermatozoa analysis. The percentage body weight gained weekly and the relative weight of the testes reduced significantly (p < 0.05) in the treatment groups. The spermatozoa analysis showed decreases in the treatment groups. In the testis and epididymis, various antioxidant parameters such as superoxide dismutase and glutathione-S-transferase were affected. The histopathology results confirmed the biochemical findings. The study suggests that EGME exerts deleterious effects on the testes and epididymes by increasing the oxidative load in rats.Keywords: Ethylene glycol monomethyl ether, Antioxidant defense, Spermatozoa, epididymes, testesNiger. J. Physiol. Sci. 33(December 2018) 195-20

Evaluation of days-dependent chloramphenicol dosage on rat liver microsomal lipid peroxidation and catalase activity

Drugs and chemical agents can alter the cellular functions associated with the oxidative metabolism, thereby stimulating ROS production. The objective of the this study was the in vivo study of the inhibitory effect of chloramphenicol on hepatic microsomal enzyme system and the effect on lipid peroxidation using the thiobarbituric acid (TBA) reactive as index of peroxidation damage was investigated. The rats were randomly divided into 3 groups; group 1 serves as the control receiving saline water, group 2 receive chloramphenicol at a dose of 28.6 mg/kg body weight/day for 5 days and group 3 for 7 days. Liver protein content, lipid hydroperoxides and catalase activity were all determined. TBARS concentration increased statistically significantly with time of exposure. After 5 days of treatment, the level of TBARS increased by 103.56% with exogenous oxidant and by 141.54% for without oxidant, as compared to the respective control. On day 7, TBARS level in the liver was approximately 90.75% higher than in the control group with oxidant and 117.03% higher than the control without oxidant. The antibiotic elicited significant increase in rat liver lipid peroxidation compared to control. There were decreases in microsomal protein content of the liver in the drug-treated rats when compared with the control rats. It also showed that chloramphenicol treatment affects cytosolic catalase activities. It decreases catalase levels by 15.75% in 5 days dosage treatment and 17.81% in 7 days dosage treatment respectively. There were significance difference (P<0.05) in the treated and control irrespective of the days of dosage. The catalase level in hepatocyte in 5 days and 7 days group was significance at p<0.01. In conclusion, it was evident that treatment of rats for 5 days and 7 days with the therapeutic doses of Chloramphenicol altered antioxidant system and the intensity of effects was concentration/dosage days dependent, it resulted in membrane lipid peroxidation, protein damage, and inhibition of microsomal catalase due to increased generation of free radicals, reactive oxygen species and reactive nitrogen speciesKeywords: Chloramphenicol, rat liver, lipid peroxidation, catalase activity, antioxidan