Serum zinc levels and body composition variability as trajectory for hyperlipidemic and dyslipidemic effect among welders exposed to welding fumes and smoking: A biomarker for cardiovascular health.

Welding is a common method for joining metals by heating them to the welding temperature. Exposure to welding fumes has a serious effect on the health of welders. This study examined serum zinc variability and body composition as route for hyperlipidemia and dyslipidemia in welders exposed to welding fumes and smoking, exploring the possibilities for the risk of possible cardiovascular disease. The experimental case control design was adopted in the study. Forty apparently healthy adult males were randomly selected comprising of twenty control group (non-smokers and smokers without welding experience) and twenty experimental group (non-smokers and smokers with welding experience) welders. Data obtained were represented as Mean ± SEM while comparison of means across group was done by one-way ANOVA followed by Tukey's multiple comparison for post hoc test at p-value < 0.05 level of significance using Graph Pad prism version 8. The data obtained showed that the body mass index (BMI) of smokers (non-welders and welders) were slightly reduced while that of non-smoking welders was increased compared to the control. The serum zinc level increased among the smoking welders, while the smoking non-welders and non-smoking welders decreased when compared to the control group (p < 0.05). Exposure to welding fumes has been shown to increase total cholesterol levels compared to the control. Weld fumes significantly (p < 0.05) increased high-density lipoproteins (HDL) levels among smoking non-welders compared to the control group, while, HDL was reduced in non-smoking welders and smoking welders, respectively (p < 0.05). Triglyceride levels significantly (p < 0.05) increased in all experimental groups compared to control levels (p < 0.05). Exposure to welding fumes and smoking caused significant changes in serum zinc, HDL and triglycerides levels with implications for the formation of plaques around the arteries interfering with the effective flow of blood through the vascular system, with implications of hyperlipidemia and dyslipidemia. This study recommends that further studies should be done using biomarkers from urine or toe nails.

Ginkgo biloba supplement abates lead-induced endothelial and testicular dysfunction in Wistar rats via up-regulation of Bcl-2 protein expression, pituitary-testicular hormones and down-regulation of oxido-inflammatory reactions.

BACKGROUND: Apoptotic and oxido-inflammatory pathways have been found to be up-regulated in lead acetate poisoning which has been associated to endothelial and testicular dysfunctions. It is yet uncertain, nevertheless, if treatment with Ginkgo biloba supplements (GBS), a flavonoid-rich natural product can lessen the adverse effects of lead on endothelial and testicular functions. This study investigated the impact of Ginkgo biloba supplementation on lead-induced endothelial and testicular dysfunctions. METHODS: The animals were treated with GBS (50 mg/kg and 100 mg/kg orally) for 14 days following oral exposure to lead acetate (25 mg/kg) for 14 days. After euthanasia, blood samples, epididymal sperm, testes, and aorta were collected. The quantities of the hormones (testosterone, follicle stimulating hormone (FSH) and luteinizing hormone (LH), as well as the anti-apoptotic, oxidative, nitrergic, inflammatory markers, were then determined using immunohistochemistry, ELISA, and conventional biochemical methods. RESULTS: GBS reduced lead-induced oxidative stress by increasing the levels of the antioxidant enzymes catalase (CAT), glutathione (GSH), and superoxide dismutase (SOD), while lowering malondialdehyde (MDA) in endothelium and testicular cells. Normal testicular weight was restored by GBS which also decreased endothelial endothelin-I and increased nitrite levels. TNF-α and IL-6 were decreased while Bcl-2 protein expression was enhanced. Lead-induced alterations in reproductive hormones (FSH, LH, and testosterone) were also restored to normal. CONCLUSION: According to our result, using Ginkgo biloba supplement prevented lead from causing endothelial and testicular dysfunction by raising pituitary-testicular hormone levels, boosting Bcl-2 protein expression and lowering oxidative and inflammatory stress in the endothelium and testes.

Preventive putative mechanisms involved in the psychopathologies of mice passively coping with psychosocial defeat stress by quercetin.

Derangements of neuroimmune, neurotrophic and neurochemical homeostasis have important implications in psychosocial stress-induced psychopathologies. Whether quercetin, a neuroactive compound, protects against psychosocial stress-induced psychiatric disturbances particularly via neurochemical mechanisms remain less well elucidated. Therefore, we further investigated the putative neurochemical as well as other cellular mechanisms of quercetin on social-defeat stress (SDS) model of psychosocial impairments. Saline (10 mL/kg,i.p.), quercetin (25, 50 and 100 mg/kg,i.p.) and ginseng (50 mg/kg,i.p.) were given to intruder mice for 14 days. From days 7-14, ten minutes of aggressive-resident-induced SDS (physical and psychological) were conducted thirty minutes after treatments. Subsequently, behavioral assessments: open-field, light/dark board, Y-maze, novel-object recognition, social-interaction and tail-suspension tests were conducted on day 14. Adrenal weight and glucose levels were measured. Monoamines, brain-derived neurotrophic factor (BDNF), corticosterone, inflammatory cytokines (TNF-α, IL-6) and executioner caspase-3 concentrations were determined in specific brain regions by ELISA. Oxidative/nitrergic stress and cholinergic markers were determined with UV-spectrophotometry. Psychosocial stress-induced anxiety, depression and cognitive defects were improved by quercetin. The decreased serotonin in the prefrontal-cortex and dopamine in the striatum, elevated levels of noradrenaline and acetylcholinesterase in the prefrontal-cortex and hippocampus with corresponding decrease in BDNF were reversed by quercetin. Quercetin reduced SDS-induced increased neuronal inflammation, caspase-3 activity, malondialdehyde, nitrite levels, but increased antioxidant activities in the three brain regions. Adrenal hypertrophy, increased serum glucose and corticosterone release were reduced by quercetin. Our findings showed that quercetin attenuates psychosocial stress-induced passive coping behavior via normalization of HPA-axis, modulation of neurochemical release, enhancement of BDNF, and inhibition of brain oxidative/nitrergic stress, neuroinflammation and apoptotic pathway.

Cabbage juice protect against lead-induced liver and kidney damage in male Wistar rat.

AIM: Liver and kidney has been implicated in Lead toxicity and this has been linked to oxidative damage. On the other hand, cabbage is one of the widely consumed vegetables with a plethora of health benefits. This present study investigated the protective effect of cabbage juice on lead-induced toxicity in male Wistar rats. METHODS: Twenty male Wistar rats were randomly divided into four groups (n = 5) and were treated with distilled water (1 ml/100 g b.wt), Lead acetate (25 mg/kg b.wt), cabbage juice (1 ml/100 g b.wt) and Lead acetate plus cabbage juice respectively. All treatments were administered orally for 28 days. Following euthanasia, blood was collected and serum decanted for biochemical assay and liver and kidney tissues were harvested, prepared for antioxidant activity and histological study. RESULT: Cabbage juice significantly attenuated Lead-induced liver and kidney dysfunction by lowering serum concentrations of urea, creatinine, ALP, AST and ALT. Antioxidants (SOD, CAT, GSH) were also upregulated in liver and kidney tissues. Cabbage juice restored the histoarchitectural changes caused by lead intoxication. CONCLUSION: Cabbage juice consumption protected the liver and kidney against lead-induced toxicity by enhancing in vivo anti-oxidant defense system.

COVID-19 pandemic: the implications of the natural history, challenges of diagnosis and management for care in sub-Saharan Africa.

BACKGROUND: Coronavirus disease (COVID-19) is a severe acute respiratory infection which has afflicted virtually almost all nations of the earth. It is highly transmissible and represents one of the most serious pandemics in recent times, with the capacity to overwhelm any healthcare system and cause morbidity and fatality. MAIN CONTENT: The diagnosis of this disease is daunting and challenging as it is dependent on emerging clinical symptomatology that continues to increase and change very rapidly. The definitive test is the very expensive and scarce polymerase chain reaction (PCR) viral identification technique. The management has remained largely supportive and empirical, as there are no officially approved therapeutic agents, vaccines or antiviral medications for the management of the disease. Severe cases often require intensive care facilities and personnel. Yet there is paucity of facilities including the personnel required for diagnosis and treatment of COVID-19 in sub-Saharan Africa (SSA). It is against this backdrop that a review of key published reports on the pandemic in SSA and globally is made, as understanding the natural history of a disease and the documented responses to diagnosis and management is usually a key public health strategy for designing and improving as appropriate, relevant interventions. Lead findings were that responses by most nations of SSA were adhoc, paucity of public health awareness strategies and absence of legislations that would help enforce preventive measures, as well as limited facilities (including personal protective equipment) and institutional capacities to deliver needed interventions. CONCLUSION: COVID-19 is real and has overwhelmed global health care system especially low-income countries of the sub-Sahara such as Nigeria. Suggestions for improvement of healthcare policies and programs to contain the current pandemic and to respond more optimally in case of future pandemics are made herein.

Altered gestational outcomes and delayed pubertal onset in prenatally and early postnatally food restricted male and female rats: mitigation by quercetin and kaempferol.

Nutrigenomic malnutrition during pregnancy and early postnatal life has serious consequences on original organ-programing, growth pattern, puberty and quality of life. The aim of this was to investigate the effect of two notable flavonoids, quercetin and kaempferol, with nutrigenomic potentials on prenatal and early postnatal food restrictions or both on gestational outcomes and the onset of puberty in male and females Wister rats. In three sets of experiments consisting of prenatal, postnatal food deprivations or both, rats were distributed into various treatment groups (n = 6). Prenatal food restriction (PrNFR) was initiated by 50% of ad libitum available diet in pregnancy (days 1-22) simultaneously with quercetin (50, 100 and 200 mg/kg, p.o./day) or kaempferol (50, 100 and 200 mg/kg, p.o./day) until delivery. However, postnatal food restriction (PsNFR) was simulated by litter-increment to 16 pups per mother from postnatal day 2 together with quercetin (50-200 mg/kg, p.o.) or kaempferol (50-200 mg/kg, p.o.) treatments until weaning (day 24) respectively. The last experiment encompasses both protocols with similar treatment protocols. Kaempferol attenuated PrNFR-induced alterations in gestational length compared to PrNFR-control. Quercetin and kaempferol significantly (P < 0.05) normalized nose-length of pups of rats exposed to PrNFR. Quercetin and kaempferol reduced the number of stillbirths due to PrNFR. Both also reduced the delay in pubertal onset as evidenced by normal onset of balanopreputial-separation and vaginal-opening in the PrNFR, PsNFR and PrNFR-PsNFR male and female rats respectively. Together, quercetin and kaempferol prevents prenatal and postnatal malnutrition-induced altered gestational outcomes and pubertal delays in rats.

Prenatal and early postnatal food restrictions cause changes in brain oxidative status and orexigenic/anorexigenic hormones in the offspring of rats: prevention by quercetin and kaempferol.

Brain oxidative signaling pathways have been identified as important targets for alleviating food deprivation-induced changes in metabolic gate-ways. Previous studies have shown that prenatal and early postnatal malnutrition alters leptin and ghrelin signaling via oxidative pathways. Thus, it has been hypothesized that agents with antioxidant properties might be beneficial for the mitigation of prenatal and early postnatal food scarcity-induced oxidative damage. Quercetin and kaempferol are natural bioflavonoids with proven antioxidant properties. In this study, we evaluated their effects on prenatal maternal food consumption, maternal and pup weights, biomarkers of orexigenic and anorexigenic hormones and oxidative stress in rats. Rats were allotted into different treatment groups (n â€‹= â€‹6) in three different experiments (prenatal, postnatal food-deprivations or both). Prenatal-food restriction (PrNFR) was induced by 50% of ad libitum accessible diet during pregnancy till parturition and postnatal-food restriction (PsNFR) was simulated by litter-enlargement to 16 pups per mother from postnatal day (PND) 2. Rats in each experiment were concurrently treated with vehicle (10 â€‹mL/kg), quercetin (50, 100 and 200 â€‹mg/kg, p.o.) or kaempferol (50, 100 and 200 â€‹mg/kg, p.o.) respectively. A third experimental group consisted of both protocols. Quercetin and kaempferol dose-dependently increased the body weights of pups exposed to PrNFR, PsNFR and PrNFR-PsNFR at PNDs 1-22 respectively. Both compounds increased maternal body weights but attenuated maternal food-intake at prenatal days 7 and 14 due by PrNFR. Quercetin and kaempferol reduced brain malondialdehyde concentrations and increased glutathione levels in PrNFR, PsNFR and PrNFR-PsNFR-exposed offspring of rats. Importantly, quercetin and kaempferol significantly (p â€‹< â€‹0.05) prevented PrNFR-, PsNFR- or PrNFR-PsNFR-induced alterations in leptin and ghrelin levels. Cumulatively, quercetin and kaempferol increased pup and maternal weights and attenuated maternal food-intake of rats submitted to PrNFR, PsNFR and PrNFR-PsNFR respectively, likely via nutrigenomic modulations of orexigenic/anorexigenic hormones and inhibition of brain oxidative stress.