Antibacterial activity of flavonoid extracts from Enteromorpha intestinalis and Caulerpa prolifera against multidrug-resistant foodborne bacterial isolates.

Background: Food poisoning caused by bacterial agents is a worldwide problem, usually accompanied by unpleasant symptoms and may be severe leading to death. Natural compounds from marine algae namely flavonoids may play a role in the remedy of this condition. Aim: This research aims to assess the potency of flavonoids extracted from Enteromorpha intestinalis and Caulerpa prolifera as antibacterial agents. Methods: Enteromorpha intestinalis was collected from Western Libyan Coast and C. prolifera was collected from Farwa Island. The antimicrobial activity and determination of minimum inhibitory concentration of algal flavonoid-containing extracts was performed in vitro against some positive and negative Gram bacteria. Results: Crude extract containing flavonoids from E. intestinalis was more effective than C. prolifera extract against Staphylococcus aureus with antimicrobial essay (25-28 + 1 and 14.5-37.5 + 0.5-1.5), MIC (50 and 50-250 µg/ml), MBC (75 and 75-250 µg/ml). In Bacillus cereus, the antimicrobial assay (19-24.5 + 0.5-1.5: 24 + 1), MIC (50-250 + 100 µg/ml), and MBC (250 and 125 µg/ml). On the other hand, flavonoids containing extract from C. prolifera were more effective than E. intestinalis against Enterohemorrhagic Escherichia coli O157 EHEC O157 (25-28 + 1: 14-18.5 + 0.5-1.5), MIC (100-250:100-500 µg/ml), and MBC (150-250 and 250-500 µg/ml). Salmonella enterica qualitatively combat by flavonoid from E. intestinalis (13.5-14 + 0.5-1: 10.5-13.5 + 0.5-1.5), MIC (100-250: 250 µg/ml), and MBC (100-250: 250 µg/ml). Flavonoids from C. prolifera (4 strains: 2 strains) were effective against S. enterica. Crude flavonoids from both algae were not effective against Bacillus pumilus. Conclusion: Data from this study could conclude that flavonoid extracts from E. intestinalis and C. prolifera could be used against foodborne bacterial agents.

Nigella sativa Oil Alleviates Mouse Testis and Sperm Abnormalities Induced by BPA Potentially through Redox Homeostasis.

BACKGROUND & AIM: Significant evidence indicates that endocrine disrupted bisphenol A (BPA) seriously endangers human health. In males, BPA affects testis architecture and sperm quality, and ultimately reduces fertility. This study explored the therapeutic potential of Nigella sativa (NS) seed extract on testis and sperm abnormalities in BPA-exposed mice and characterized the underlying mechanism. METHODS: Forty male Swiss albino mice (5.5 weeks old, N = 8 per group) were randomly divided into five groups: Group I, normal control, Group II, vehicle control (sterile corn oil); Group III, NS-exposed (oral 200 mg/kg); Group IV, BPA-exposed (oral 400 µg/kg body weight); Group V, BPA + NS-exposed mice. Animals were treated for 6 weeks and sacrificed for biochemical and histological examination. RESULTS: The results indicated that BPA exposure results in significant testis and sperm abnormalities. Specifically, BPA promoted a marked reduction in the body and testis compared with the control group. Histopathological findings showed that BPA caused a widespread degeneration of spermatogenic cells of the seminiferous epithelium, decreased sperm counts and motility, and augmented sperm abnormalities, and whereas little alteration to sperm DNA was observed. In addition, BPA increased the levels of the lipid peroxidation marker, malondialdehyde (MDA), and reduced the levels of the antioxidant marker, reducing glutathione (GSH). Treatment with NS oil extract during BPA exposure significantly alleviated testis and sperm abnormalities, reduced MDA levels, and enhanced GSH levels. CONCLUSION: The results demonstrate that NS oil protects mice against BPA-induced sperm and testis abnormalities, likely by suppressing levels of the oxidative stress marker, MDA, and enhancing the levels of the antioxidant marker, GSH.

Selective adenosine A2A receptor inhibitor SCH58261 reduces oligodendrocyte loss upon brain injury in young rats.

Cellular elements of maturing brain are vulnerable to insults, which lead to neurodevelopmental defects. There are no established treatments at present. Here we examined the efficacy of selective adenosine A2A receptor inhibitor SCH58261 to combat brain injury, particularly oligodendrocyte (OL) lineage cells, in young rats. Wistar rats (n = 24, 6.5 days old) were randomly divided into equal groups of four. The sham (SHAM) group received no treatment, the vehicle (VEHICLE) group received 0.1% dimethylsufoxide, the injury (INJ) group was exposed to oxygen-glucose deprivation insult, and the injury+SCH58261 (INJ+SCH58261) group was exposed to the insult and received 1 µM SCH58261. Immunocytochemical experiments revealed that there was a significant reduction in the populations of mature OL (MBP+ OLs) and immature OL precursors (NG2+ OPCs) in the INJ group compared to SHAM group. Furthermore, there was also a significant increase in the percent of apoptotic MBP+ OL and NG2+ OPC populations as evidenced by TUNEL assay. In addition, there was a significant reduction in the proliferation rate among NG2+ OPCs, which was confirmed by BrdU immunostaining. On the other hand, treatment with SCH58261 significantly enhanced survival, evidenced by the reduction in apoptotic indices for both cell types, and it is preserved the NG2+ OPC proliferation. Activation of adenosine A2A receptors may contribute to OL lineage cell loss in association with decreased mitotic behavior of OPCs in neonatal brains upon injury. Future investigations assessing ability of SCH58261 to regenerate myelin will provide insights into its wider clinical relevance.

Paternal bisphenol A exposure induces testis and sperm pathologies in mice offspring: Possibly due to oxidative stress?

Bisphenol A (BPA), an endocrine and metabolic disruptor, is widely used to manufacture polycarbonate plastics and epoxy resins. Accumulating evidence suggests that paternal BPA exposure adversely affects male germlines and results in atypical reproductive phenotypes that might persist for generations to come. Our study investigated this exposure on testicular architecture and sperm quality in mouse offspring, and characterised underlying molecular mechanism(s). A total of 18 immature male Swiss albino mice (3.5 weeks old) were randomly divided into three groups and treated as follows: Group I, no treatment (sham control); Group II, sterile corn oil only (vehicle control); Group III, BPA (400 µg/kg) in sterile corn oil. At 9.5 weeks old, F0 males were mated with unexposed females. F0 offspring (F1 generation) were monitored for postnatal development for 10 weeks. At 11.5 weeks old, the animals were sacrificed to examine testicular architecture, sperm parameters, including DNA integrity, and oxidative stress biomarkers. Results showed that BPA significantly induced changes in the body and testis weights of the F0 and F1 generation BPA lineages compared to F0 and F1 generation control lineages. A decrease in sperm count and motility with further, increased sperm abnormalities, no or few sperm DNA alterations and elevated levels of MDA, PC and NO were recorded. Similar effects were found in BPA exposed F0 males, but were more pronounced in the F0 offspring. In addition, BPA caused alterations in the testicular architecture. These pathological changes extended transgenerationally to F1 generation males' mice, but the pathological changes were more pronounced in the F1 generation. Our findings demonstrate that the biological and health BPA impacts do not end in paternal adults, but are passed on to offspring generations. Hence, linking observed testis and sperm abnormalities in the F1 generation to BPA exposure of their parental line was evident in this work. The findings also illustrate that oxidative stress appears to be a molecular component of the testis and sperm pathologies.

Determination of metals as bio indicators in some selected bee pollen samples from Jordan.

This study was done to determine the degree of metals and heavy metals in some bee pollen sample as biological indicator for environmental pollution. Sample were collected from industrial, urban and agricultural areas of Jordan in year 2017. Eight metals (As, Cd, Cu, Mg, Pb, Ni, Se, and Zn) continents analyzed by using Inductively Coupled Plasma Optical Emission Spectrum, (ICP-OES). Results were statistically interpreted by using ANOVA analysis. Metals content in bee pollen from Jordan and China were determined within the following ranges (minimum-maximum mg/kg); Cu (copper): 11.338-0.032, Zn (Zinc): 77.022-25.24, Ni (Nickel): 2.839 to <0.01, Se (Selenium): 3.03 to <0.04, Mg (Magnesium): 1575.19-641.388, Pb (Lead): 2.567 to <0.03, Cd (Cadmium): <0.005, As (Arsenic): <0.02. The results showed that there were no statistically significant differences among metals in the bee pollen. It has also found that bee pollen produced in Jordan may be a good source of some trace elements like Se and Mg and can be used as an environmental indicator and for quality control.

Environmentally toxicant exposures induced intragenerational transmission of liver abnormalities in mice.

Environmental toxicants such as chemicals, heavy metals, and pesticides have been shown to promote transgenerational inheritance of abnormal phenotypes and/or diseases to multiple subsequent generations following parental and/or ancestral exposures. This study was designed to examine the potential transgenerational action of the environmental toxicant trichloroethane (TCE) on transmission of liver abnormality, and to elucidate the molecular etiology of hepatocyte cell damage. A total of thirty two healthy immature female albino mice were randomly divided into three equal groups as follows: a sham group, which did not receive any treatment; a vehicle group, which received corn oil alone, and TCE treated group (3 weeks, 100 µg/kg i.p., every 4th day). The F0 and F1 generation control and TCE populations were sacrificed at the age of four months, and various abnormalities histpathologically investigated. Cell death and oxidative stress indices were also measured. The present study provides experimental evidence for the inheritance of environmentally induced liver abnormalities in mice. The results of this study show that exposure to the TCE promoted adult onset liver abnormalities in F0 female mice as well as unexposed F1 generation offspring. It is the first study to report a transgenerational liver abnormalities in the F1 generation mice through maternal line prior to gestation. This finding was based on careful evaluation of liver histopathological abnormalities, apoptosis of hepatocytes, and measurements of oxidative stress biomarkers (lipid peroxidation, protein carbonylation, and nitric oxide) in control and TCE populations. There was an increase in liver histopathological abnormalities, cell death, and oxidative lipid damage in F0 and F1 hepatic tissues of TCE treated group. In conclusion, this study showed that the biological and health impacts of environmental toxicant TCE do not end in maternal adults, but are passed on to offspring generations. Hence, linking observed liver abnormality in the offspring to environmental exposure of their parental line. This study also illustrated that oxidative stress and apoptosis appear to be a molecular component of the hepatocyte cell injury.