Biochemical Dysfunctions Research Articles

A Review on Therapeutic Strategies against Parkinson's Disease: Current Trends and Future Perspectives.

Parkinson's Disease (PD) is the most common neurodegenerative disorder after Alzheimer's Disease and is clinically expressed by movement disorders, such as tremor, bradykinesia, and rigidity. It occurs mainly in the extrapyramidal system of the brain and is characterized by dopaminergic neuron degeneration. L-DOPA, dopaminergic agonists, anticholinergic drugs, and MAO-B inhibitors are currently used as therapeutic agents against PD, however, they have only symptomatic efficacy, mainly due to the complex pathophysiology of the disease. This review summarizes the main aspects of PD pathology, as well as, discusses the most important biochemical dysfunctions during PD, and presents novel multi-targeting compounds, which have been tested for their activity against various targets related to PD. This review selects various research articles from main databases concerning multi-targeting compounds against PD. Molecules targeting more than one biochemical pathway involved in PD, expected to be more effective than the current treatment options, are discussed. A great number of research groups have designed novel compounds following the multi-targeting drug approach. They include structures combining antioxidant, antiinflammatory, and metal-chelating properties. These compounds could be proven useful for effective multi-targeted PD treatment. Multi-targeting drugs could be a useful tool for the design of effective antiparkinson agents. Their efficacy towards various targets implicated in PD could be the key to the radical treatment of this neurodegenerative disorder.

Biochemical and pharmacological properties of a polyherbal antilipemic tea in chemically induced hyperlipidemia

The incidence of hyperlipidemia is increasing worldwide. Compared to individual herbs, polyherbal formulations have been hyped to possess increased therapeutic effectiveness due to the synergistic actions of the constituent herbs. However, the proliferation of putative herbal remedies is a cause for concern because of safety and efficacy issues. Thus, this study investigated the performance of a polyherbal tea (PHT) in Triton X-1339-induced lipid and other biochemical disorders in rats to gain insight into its safety and efficacy. PHT was screened for phytochemical, mineral, and proximate contents. Hyperlipidemia was induced in male Wistar rats by administering 200 mg/kg of Triton X-1339 to them intraperitoneally. Animals then received an infusion of PHT for two weeks. Lipid profile, organ impairment, and hematological assessments were performed on tissues excised from the experimental animals. The phytochemical screening detected polyphenols and tannins in PHT. The estimated amounts of phenols and flavonoids in PHT were 150.60 ± 1.40 mg Gallic acid equivalent and 3961.11 ± 30.06 mg Quercetin equivalent, respectively. Triton injection caused dyslipidemia, and cardiohepatorenal redox imbalance and biochemical dysfunction. The Triton-induced dyslipidemia, redox imbalance, and alterations to biochemical indices of organ function were counteracted by PHT. In addition, Triton administration showed a deleterious effect on the hematological profile of dyslipidemic rats which was corrected following their treatment with PHT. The efficacy of PHT compared well with that of Rosuvastatin. The results obtained demonstrated the apparent safety and therapeutic efficacy of PHT in hyperlipidemia and related biochemical dysfunctions.

Chronic toxicity of sediment-bound triclosan on freshwater walking catfish Clarias magur: Organ level accumulation and selected enzyme biomarker responses

Triclosan (TCS) is a biocide widely used in personal care and medicinal products. TCS persists in sediments and has been detected worldwide, making sediments a vital route of TCS exposure to aquatic organisms. This experiment explored the bioaccumulation and toxicological effects of TCS-contaminated sediment. The study revealed that the half-life of TCS in the sediment-water system was 21.52 days. Exposure of Clarias magur juveniles to 0.4 and 0.8 mg kg−1 TCS-spiked sediment resulted in high Biota-Sediment Accumulation Factor (BSAF) with the highest bioaccumulation in the liver (29.62–73.61 mg kg−1), followed by gill (9.22–17.57 mg kg−1), kidney (5.04–9.76 mg kg−1), muscle (2.63–4.87 mg kg−1) and brain (1.53–3.20 mg kg−1). Furthermore, a concentration-dependent increase in oxidative stress biomarkers such as superoxide dismutase (SOD), catalase (CAT) and glutathione-S-transferase (GST) was documented during 45 days of exposure in gill, liver, kidney, muscle, and brain tissues of exposed fish. A similar increasing trend was also recorded for liver transaminase enzymes such as glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) during the experimental period compared to control. Serum biochemical analysis revealed a significant time and concentration-dependent increase in serum glucose, serum GOT, and serum GPT, while serum total protein and albumin decreased significantly during exposure. These findings demonstrate high bioaccumulative and toxic nature of TCS in fish, promoting multiple physiological and biochemical dysfunctions through sediment exposure. The study underscores the urgent need for strengthened regulations and robust monitoring of triclosan across various environmental matrices, including sediment, to mitigate the detrimental impacts of TCS effectively.

Variants in Human ATP Synthase Mitochondrial Genes: Biochemical Dysfunctions, Associated Diseases, and Therapies.

Mitochondrial ATP synthase (Complex V) catalyzes the last step of oxidative phosphorylation and provides most of the energy (ATP) required by human cells. The mitochondrial genes MT-ATP6 and MT-ATP8 encode two subunits of the multi-subunit Complex V. Since the discovery of the first MT-ATP6 variant in the year 1990 as the cause of Neuropathy, Ataxia, and Retinitis Pigmentosa (NARP) syndrome, a large and continuously increasing number of inborn variants in the MT-ATP6 and MT-ATP8 genes have been identified as pathogenic. Variants in these genes correlate with various clinical phenotypes, which include several neurodegenerative and multisystemic disorders. In the present review, we report the pathogenic variants in mitochondrial ATP synthase genes and highlight the molecular mechanisms underlying ATP synthase deficiency that promote biochemical dysfunctions. We discuss the possible structural changes induced by the most common variants found in patients by considering the recent cryo-electron microscopy structure of human ATP synthase. Finally, we provide the state-of-the-art of all therapeutic proposals reported in the literature, including drug interventions targeting mitochondrial dysfunctions, allotopic gene expression- and nuclease-based strategies, and discuss their potential translation into clinical trials.

Epilepsy in Stroke as De Novo Independent Nosology Unit – Physiology, Pathogenesis, Histology, Clinical Picture, Diagnosis, and Treatment – A Systematic Review

INTRODUCTION: Early seizures are considered complications of stroke, and late seizures are a type of structural epilepsy. If they are separated as a new independent nosology unit, the problem in the diagnostic – treatment approach will be solved. PHYSIOLOGY: Cerebral blood flow is regulated by local factors such as carbon dioxide and oxygen content. Brain activity is also an important factor in the regulation of the volume speed of the blood – with locally increased neuronal activity, the local blood flow increases. Neurons in the CNS are subject to a variety of effects mediated by membrane receptors of two types – ionotropic and metabotropic. PATHOGENESIS: Early seizures are due to transient biochemical dysfunctions, while late seizures are due to gliosis changes affecting neuronal excitability. HISTOLOGY: The highlighted histopathological aspects confirm and support the results of clinical and radiological studies with dead nervous tissue, replaced by numerous newly formed capillaries, and surrounded by lipid-laden macrophages. CLINICAL PICTURE: This is represented by a complex combination of excitatory epileptic manifestations and residual focal symptoms depending on the localization of the lesion. LABORATORY DIAGNOSTICS: A very typical group of patients with post-stroke seizures have a high risk of recurrence when some of the studied biomarkers for this are available in the blood. In summary, the additional expanded package of studies of stroke patients should include screening diagnostics for the risk of epileptic seizures, namely: IL-6, IL-1β, TNF, Mg2+, Ca2+, CD40L, and Hsc70. IMAGING: Transient periodic MRI abnormalities have been demonstrated, possibly as a result of cerebral edema induced by seizure activity. Routine MRI in stroke patients is recommended. TREATMENT: It is possible that rt-PA may increase the risk of early seizures after stroke. Levetiracetam (LEV) as a neuroprotective agent in stroke has been proposed as the drug of first choice, based on safety and efficacy profiles. The usual practice is to treat recurrent early-onset seizures with short-term (3–6 months) treatment with antiepileptic drugs. CONCLUSIONS: Separation of stroke-epilepsy as a new independent nosology entity will solve the diagnostic-treatment problems in this area by changing the minimum package for laboratory tests, as well as routine MRI in patients with clinical evidence of stroke. LEV is the first-line agent for the treatment of these patients, in combination with correction of registered laboratory parameters.

Metabolomic Changes as Key Factors of Green Plant Regeneration Efficiency of Triticale In Vitro Anther Culture

Green plant regeneration efficiency (GPRE) via in vitro anther culture results from biochemical pathways and cycle dysfunctions that may affect DNA and histone methylation, with gene expression influencing whole cell functioning. The reprogramming from gametophytic to sporophytic fate is part of the phenomenon. While DNA methylation and sequence changes related to the GPRE have been described, little attention was paid to the biochemical aspects of the phenomenon. Furthermore, only a few theoretical models that describe the complex relationships between biochemical aspects of GPRE and the role of Cu(II) ions in the induction medium and as cofactors of enzymatic reactions have been developed. Still, none of these models are devoted directly to the biochemical level. Fourier transform infrared (FTIR) spectroscopy was used in the current study to analyze triticale regenerants derived under various in vitro tissue culture conditions, including different Cu(II) and Ag(I) ion concentrations in the induction medium and anther culture times. The FTIR spectra of S-adenosyl-L-methionine (SAM), glutathione, and pectins in parallel with the Cu(II) ions, as well as the evaluated GPRE values, were put into the structural equation model (SEM). The data demonstrate the relationships between SAM, glutathione, pectins, and Cu(II) in the induction medium and how they affect GPRE. The SEM reflects the cell functioning under in vitro conditions and varying Cu(II) concentrations. In the presented model, the players are the Krebs and Yang cycles, the transsulfuration pathway controlled by Cu(II) ions acting as cofactors of enzymatic reactions, and the pectins of the primary cell wall.

Thyroid stimulating hormone (thyrotrophin) and its relationship with chronic kidney disease before dialysis.

Objective: To measure glomerular filtration rate, free thyroxin, and thyrotrophin in chronic kidney disease patients and to find out the correlation between glomerular filtration rates, free thyroxin and thyrotrophin in these patients. Study Design: Cross Sectional Analytical study. Setting: Bacha Khan Medical Complex Swabi. Period: November 2018 to November 2019. Material & Methods: Sixty five patients were included in the study. Serum Creatinine, TSH and Free T4 were measured; Thyroid function tests TSH, FT4 were measured in these chronic kidney disease patients through enzyme linked immunosorbant assay method. GFR was calculated through Cock-croft-Gualt formula and the relevant data was entered in a predesigned Proforma. Results: In the study total 65 chronic kidney disease patients were taken. Out of which thirty six (55.4%) were male and twenty nine (44.6%) were female. Thirty five (53.8%) CKD patients whose TSH level was above the normal limit while in the remaining patients the TSH values were in the normal range. Eight patients (12.3%) out of sixty five patients in whom FT4 values were below the normal limit while in the remaining fifty seven patients (87.6%) FT4 values were within the reference range. Those eight patients whose FT4 was below the normal value, their TSH values were above the normal value too. Thirty five patients, whose TSH levels were above the normal limit, their mean age was 50.60± 11.95, mean serum creatinine was 4.73± 2.94 mg/dl, mean GFR was 22.17± 12.48 ml/min/1.73m2, mean TSH was 6.68± 0.87 mIU/L and mean FT4 was 0.97± 0.35 ng/dl. The p-value of TSH was < 0.001 and FT4 was < 0.05 in comparing with control group. Glomerular filtrations rate with TSH and FT4 the co-efficient of correlation (r) value for 35 patients was – 0.713 and 0.47 for TSH and FT4 respectively. Their p- values were 0.000 and 0.004 respectively, and p < 0.001 collectively. This was found to be statistically significant. Linear regression line was obtained between GFR and FT4 in CKD patients. Conclusion: chronic kidney disease is associated with biochemical thyroid dysfunctions causing most commonly subclinical hypothyroidism.

Ameliorating Effect of Morin Hydrate on Chronic Restraint Stress-induced Biochemical Disruption, Neuronal, and Behavioral Dysfunctions in BALB/c Mice.

Morin hydrate (MH) is a bioflavonoid component of many fruits and vegetables. Our previous research demonstrated that MH provides neuroprotection in mouse models of acute restraint stress and sleep deprivation by attenuating hippocampal neuronal damage and enhancing memory. Based on these findings, our study investigated the role of MH in chronic stress-induced neuronal and biochemical perturbations in BALB/c mice. Male BALB/c mice were divided into 6 groups (n=6). Groups 1 and 2 received vehicle (10 mL/kg normal saline), groups 3-5 received MH (5, 10, 20 mg/kg IP), while group 6 received ginseng (25 mg/kg) daily and 30 minutes afterward were restrained in a plastic cylindrical restrainer for 14 days. Immobility time in the forced swim test increased in the MH-treated group, indicating an antidepressant-like effect. Also, a reduction in frequency and duration of open arms exploration was observed in the elevated plus-maze (EPM) test in stressed mice, and administration of MH (5, 10, 20 mg/kg, IP) reversed these effects. An increase in blood levels of glucose, triglycerides, total cholesterol, and brain malondialdehyde and nitrite levels was observed in the stressed groups, which was reversed by MH. Furthermore, MH reversed the stress-induced reduction in HDL cholesterol and glutathione (GSH) levels and attenuated stress-induced alterations in the prefrontal cortex and hippocampus. Our findings suggest that MH attenuated chronic restraint stress-behavioral and biochemical perturbations, probably due to its capability to decrease oxidative stress and brain neuronal damage. Chronic stress perturbs physiological and psychological homeostasis;Morin hydrate normalized chronic stress-induced biochemical disruptions;Morin hydrate attenuated structural changes in prefrontal cortex and hippocampus. Stress is a state of being overwhelmed by demands exceeding the personal and social means of coping. Exposure to excessive stress has resulted in disruption of neurochemical and physiological processes, which sometimes manifest as behavioural abnormalities. Therefore to cope with the stressful life style, there is need to develop a therapeutic agent of plant origin. Morin hydrate is a flavonoid with known antioxidant and neuroprotective properties; however, its effect in a stressful condition has not been studies. The study thus evaluated ameliorating effect of Morin hydrate on chronic restraint stress-induced biochemical disruption, neuronal and behavioral dysfunctions in BALB/c mice. To achieve this, mice were exposed to chronic restraint stress protocol for fourteen days. Behavioural changes were examined using various techniques. The vital parameters like antioxidant, glucose and nitrite levels were also taken. Our findings show that Morin hydrate prevented behavioral abnormalities and damage to the brain cells. It also inhibited stress-induced biochemical disturbance.

SCREENING TESTS FOR THYROID DYSFUNCTION; IS TSH SUFFICIENT?

There are different recommendations on how to screen for thyroid gland problems and TSH is the most ordered test. Anti TPO antibodies are usually tested when TSH is not within the normal range, but their presence before TSH changes has not been appreciated. This study aims to evaluate the role of anti-TPO and thyroid ultrasound for the early detection of thyroid pathologies, especially in the subclinical phase. This is a cross-sectional study in 458 individuals (80% females and 20% males). Thyroid laboratory tests and thyroid ultrasound was done. Statistical analysis was performed to assess the prevalence of thyroid dysfunction, thyroid antibodies and their correlation with thyroid ultrasound changes. 88.6 % (406) of subjects resulted in euthyroid. Subclinical hypothyroidism and hyperthyroidism were observed in 5.5% and 1.7% of the population, respectively. The prevalence of positive thyroid antibodies was 26.5% in females and 11.8 % in males. Hypoechoic structure, heterogenicity and micronodular pattern in ultrasound were associated with significantly higher TPO antibodies activity p<.001. Undiagnosed biochemical thyroid dysfunctions were common in our country. Measurement of anti-TPO in individuals with normal TSH is valuable in determining individuals at risk for thyroid pathologies.

SCREENING TESTS FOR THYROID DYSFUNCTION; IS TSH SUFFICIENT?

There are different recommendations on how to screen for thyroid gland problems and TSH is the most ordered test. Anti TPO antibodies are usually tested when TSH is not within the normal range, but their presence before TSH changes has not been appreciated. This study aims to evaluate the role of anti-TPO and thyroid ultrasound for the early detection of thyroid pathologies, especially in the subclinical phase. This is a cross-sectional study in 458 individuals (80% females and 20% males). Thyroid laboratory tests and thyroid ultrasound was done. Statistical analysis was performed to assess the prevalence of thyroid dysfunction, thyroid antibodies and their correlation with thyroid ultrasound changes. 88.6 % (406) of subjects resulted in euthyroid. Subclinical hypothyroidism and hyperthyroidism were observed in 5.5% and 1.7% of the population, respectively. The prevalence of positive thyroid antibodies was 26.5% in females and 11.8 % in males. Hypoechoic structure, heterogenicity and micronodular pattern in ultrasound were associated with significantly higher TPO antibodies activity p<.001. Undiagnosed biochemical thyroid dysfunctions were common in our country. Measurement of anti-TPO in individuals with normal TSH is valuable in determining individuals at risk for thyroid pathologies.

High Prevalence of Anti Thyroid Antibodies in an Albanian Cohort of Patients

Introduction: Albania is classified as iodine deficient region and endemic goiter in this country has been a concern for public health. A salt iodization program has been implemented in Albania since 2008. Most of regions still remain with a mild or moderate iodine deficiency there are no studies on prevalence of thyroid autoimmune disorders. The purpose of this study was to assess thyroid function and the presence of thyroid antibodies in subjects that were not previously diagnosed or treated for thyroid disorders. Methods: This is a cross-sectional study performed in a cohort of patients in Albania during a 2 year period (january 2018-january 2020). We assessed the prevalence of thyroid function disorders and presence of thyroid antibodies in 5047 subjects (81% females and 19% males). Individuals previously diagnosed or treated for thyroid disease were excluded from the study. TSH, Free T4, total T3, Anti TPO(thyroid peroxidase) and anti TG (thyroglobulin) were measured with electrochemiluminescence method with Cobas 6000 Roche Diagnostics. We calculated the frequency of thyroid antibodies and the abnormal thyroid function. Statistical analysis was performed to see if there was a difference between individuals with positive antibodies and those negative for antibodies. Results: 91 % (4596) of subjects resulted euthyroid. We found a low prevalence of overt thyroid dysfunction (hyperthyroidism 0.48% and hypothyroidism 1.69%). The rates of subclinical hypothyroidism and hyperthyroidism were 5.5% and 1.4% respectively. The prevalence of positive thyroid antibodies, at least one of them was 28% in females and 14% in males (2:1 ratio). 97.3 % of subjects who testet negative for antibodies had normal thyroid function compared to 73.5% in antibodies positive group. There was a significant difference for subclinical hypothyroidism and other thyroid disorders between antibodies positive group and antibodies negative group (p value <0.0000119% of individuals(from 5047 examined) had normal thyroid function and resulted positive for anti TPO or anti TG. Conclusions: Undiagnosed biochemical thyroid dysfunctions were common in subjects living in a mild to moderate iodine-deficient area especially subclinical hypothyroidism. TSH level correlated well with the presence of antibodies resulting in significant difference in thyroid function between 2 groups. We found a high prevalence (19%) of thyroid antibodies in euthyroid subjects. TPO antibodies in euthyroid subjects can be used to identify subjects with increased risk for hypothyroidism such as women who are pregnant (to predict first trimester or postpartum thyroid dysfunction), patients with other autoimmune diseases, subjects on drugs like amiodarone or relatives of patients with autoimmune thyroid diseases.

Physiological responses to lead exposure in wheat, barley and oat

Lead (Pb) is an environmental pollutant extremely toxic to plants productivity and threatens human and animal health. Lead has no biological function but can cause morphological, physiological, and biochemical dysfunctions in plants. Plants have developed a wide range of tolerance mechanisms that are activated in response to lead exposure. To study the effects of lead on metabolism, four plant species, wheat (Triticum durum Desf and Triticum aestivum L.), barley (Ordeum vulgare L.) and oats (Avena sativa L.), were grown and stressed with lead acetate, Pb(CH3COO)2, at three concentrations (0.15, 0.3 and 0.6 g/l). The results indicate that lead stress affects all parameters measured. Treatment with 0.3 and 0.6 g/l of lead acetate showed an increase on total protein content in the leaves and roots of Triticum durum Desf. By contrast, the impacts of lead on soluble sugars differ between species; they are reduced in Triticum aestivum L and Ordeum vulgare L at all lead concentrations, whereas they are increased in Triticum durum Desf and Avena sativa L where their value peaks at 0.6 g/l Pb.

Therapeutic evaluation of anti-trypanosoma activity of ethanol extracts of Jatropha curcas roots in comparison with diminazene aceturate in Trypanosoma brucei brucei–parasitized rats

Jatropha curcas is used as an old herbal therapy in the treatment of several vector-borne diseases in several parts of Africa. Considering the burden of trypanosoma infection and the cost of currently available drugs, the search for more drugs that are effective, affordable and accessible is warranted. To investigate the anti-trypanosoma and ameliorative effects of ethanol extracts of Jatropha curcas root (EEJCR) on organ malfunctions associated with trypanosoma infection in rats, and its phytoconstituents and acute toxicity profile. Thirty rats were divided into six groups of rats (n = 5): nonparasitized rats in group 1 served as normal control and parasitized (1.8 × 106 trypanosomes/ml of Trypanosoma brucei brucei–infected blood) rats in group 2 served as trypanosome control. Parasitized rats in group 3 were treated with reference drug (diminazene aceturate) while groups 4–6 were treated with 100, 200 and 400 mg/kg/day b.w. p.o. of EEJCR, respectively for 7 days. The acute toxicity profile of EEJCR was established in mice using the standard method. In a dose-dependent fashion, EEJCR reduced trypanosoma parasitaemia; 400 mg/kg/day b.w. of EEJCR gave 82.96% chemosuppression compared with 100% by diminazene aceturate. EEJCR also ameliorated trypanosoma-modified haematological and biochemical dysfunctions in a dose-related manner. The presence of tannins, steroids, flavonoids, terpenoids, phenols, glycosides and alkaloids was detected in EEJCR and it was tolerable up to 5000 mg/kg b.w. This study showed that EEJCR is safe, has anti-trypanosoma activity and reverses haematological and biochemical markers of organ malfunctions associated with trypanosoma infection. This observation justifies the old routine use of such herbal therapy in medicinal practices to treat trypanosomiasis.

Testicular dysfunction in malathion induced toxicity in male rats: Protective role of NAC and Silymarin.

This study investigated the biochemical and histopathological testicular dysfunctions following subacute toxic exposure to malathion; and the potential counteracting effects of N-acetyl cysteine (NAC) and Silymarin against these induced toxic effects. The study was carried out on 48 Sprague-Dawley males, rats were divided into six equal groups, drugs were given by gastric gavage daily for 30 days as follow; control group: received distilled water, the group I: rats were treated with NAC at a dose 200 mg/kg/day; group II: rats were treated with Silymarin at a dose 200 mg/kg/day; group III: rats were given malathion at a dose of 200 mg/kg/day; group IV: rats were given malathion plus NAC; group V: rats were given malathion plus Silymarin. Significant reductions in the testicular weights were observed in malathion exposed rats. Malathion caused significant reductions in hormonal assay including follicle –stimulating hormone (FSH), luteinizing hormone (LH) and testosterone, butyryl cholinesterase activity as well, sperm counts and motility with significant increases in abnormal sperm morphology. The histopathological findings showed diffusely necrotic seminiferous tubules and arrested spermatogenesis. Administration of NAC and Silymarin improved the biochemical and histopathological alterations in the testes induced by malathion. However, NAC was much better than Silymarin for inducing these protective effects.

Toxicological and pharmacological assessment of a multiherbal phytopharmaceutical on Triton X-1339-induced hyperlipidemia and allied biochemical dysfunctions.

This study investigated the safety and therapeutic effect of a multiherbal tea (MHT) on Triton X-1339-induced hyperlipidemia and associated biochemical and tissue dysfunctions. An infusion of the MHT was assessed for phytoconstituents, proximate and mineral composition, and antioxidant activity. Wistar rats administered 200mg/kg Triton X-1399 were post-treated with MHT for 14days followed by biochemical estimations in serum, heart, liver, and kidney of animals. Hematological and histopathological evaluations of the blood, and liver, respectively, were also performed. Different phytochemicals were detected in MHT, toxic metals were absent and antioxidant activity was appreciable. Disturbances in glucose level and redox homeostasis, alterations in liver, kidney, and heart function markers, and imbalances in hematological parameters precipitated by triton toxicity were mitigated by posttreatment with MHT. Multiherbal tea also ameliorated triton-induced hepatic histoarchitectural abnormalities. These results suggest that MHT is apparently an effective antilipemic tea with minimal or no side effects. PRACTICAL APPLICATIONS: Hyperlipidemia is one of the core risk factors for arteriosclerosis and a major contributor to other adverse health conditions. The prevalence of hyperlipidemia has increased drastically in the last few decades. Plant and plant products have been extensively used in the management of dyslipidemia and many plant-based antilipemic products with poorly defined toxicity and pharmacological profiles abound in the market. The results of this study demonstrated the protective effects of a MHT against triton-induced hyperlipidemia, atherogenic tendency, and dysfunction of key organs in rats and lent credence to its therapeutic relevance in the management of hyperlipidemia and related diseases.

Modulation of key enzymes linked to Parkinsonism and neurologic disorders by Antiaris africana in rotenone-toxified rats.

Background The physiopathologies of many neurologic diseases are characterized by related biochemical dysfunctions that could be explored as drug targets. This study evaluated the effect of a methanol leaf extract of Antiaris africana (MEA) on critical bioindices of Parkinsonism and related neurologic dysfunctions in rats with rotenone-induced neurotoxicity. Methods Animals were administered 50 or 100 mg/kg MEA for 14 consecutive days. Rotenone (1.5 mg/kg) was administered three times per day on days 13 and 14. Coenzyme Q10 (5 mg/kg) was the reference drug. Complex I activity, dopamine level, activities of acetylcholinesterase, myeloperoxidase, Na+/K+ ATPase and glutamine synthetase, as well as oxidative stress indices were evaluated at the end of the period of treatment. Results Rotenone-intoxicated group showed disruption of complex 1 activity, dopamine level, and glutamine synthetase activity with negative alterations to activities of acetylcholinesterase, myeloperoxidase, and Na+/K+ ATPase as well as heightened cerebral oxidative stress. MEA restored brain mitochondria functionality, mitigated altered neurochemical integrity, and ameliorated cerebral oxidative stress occasioned by rotenone neurotoxicity. The activity of A. Africana was comparable with that of 5 mg/kg coenzyme Q10. Conclusions These results indicated that A. africana displayed therapeutic potential against Parkinsonism and related neurologic dysfunctions and support its ethnobotanical use for the treatment of neurologic disorders.

Methanol Extract of Peltophorum pterocarpum Stem Bark Has Antimalarial Activity and Normalizes Biochemical Changes Induced by Plasmodium berghei Infection

This study evaluated the antimalarial, haematological and biochemical status of Plasmodium berghei Anka 65-infected mice treated with methanol extract of Peltophorum pterocarpum stem bark (MEPT). The acute toxicity profile and phyto-constituents were also evaluated. Thirty mice were divided into 6 groups of 5 mice each. Group 1 served as normal control and received distilled water only. Group 2 was parasitized and untreated. Groups 3-5 were parasitized and treated with 200, 400 and 600 mg/kg b.w. body weight of MEPT respectively. Group 6 was parasitized and treated with 28 mg/kg. b.w. of arthemeter/lumenfantrin combination. Malaria parasitemia were monitored on treatment days 0-3. Antioxidant, liver, kidney and lipid peroxidation status were determined using classical methods 5 days post-treatment. There were dose-dependent reductions in malaria parasitemia percentages of groups 3-5 that are comparable with group 6. In addition, there were dose and duration-dependent increases in malaria chemo-suppression in groups 3-5. The existence of oxidative stress, lipid peroxidation, and kidney and liver dysfunctions were observed in group 2 when compared with group 1. Treatment of groups 3-5 with MEPT and group 6 with arthemeter/lumenfantrin for 4 days restored the biochemical anomalies induced by malaria. The extract was tolerable up to 5,000 mg/kg b.w. of MEPT. The presence of flavonoids, alkaloids, saponins, tannins, steroids, carotenoids, glycosides, anthraquinones, terpenoids and anthocyanins were detected in high amounts while phenols was detected in low amount in MEPT. These suggest that MEPT possesses antimalarial activity and normalizes malaria-modified biochemical changes. These effects might be attributed to its bioactive constituents. Keywords: malaria, Peltophorum pterocarpum, phytochemicals, toxicity, biochemical dysfunctions DOI : 10.7176/ALST/73-05 Publication date : April 30 th 2019

Effect of Chronic Administration of Nickel on Affective and Cognitive Behavior in Male and Female Rats: Possible Implication of Oxidative Stress Pathway.

Nickel (Ni) toxicity has been reported to produce biochemical and behavioral dysfunction. The present study was undertaken to examine whether Ni chronic administration can induce alterations of affective and cognitive behavior and oxidative stress in male and female rats. Twenty-four rats, for each gender, divided into control and three test groups (n = 6), were injected intraperitoneally with saline (0.9% NaCl) or NiCl2 (0.25 mg/kg, 0.5 mg/kg and 1 mg/kg) for 8 weeks. After treatment period, animals were tested in the open-field, elevated plus maze tests for anxiety-like behavior, and forced swimming test for depression-like behavior. The Morris Water Maze was used to evaluate the spatial learning and memory. The hippocampus of each animal was taken for biochemical examination. The results showed that Ni administration dose dependently increased anxiety-like behavior in both tests. A significant increase in depression-like symptoms was also exhibited by Ni treated rats. In the Morris Water Maze test, the spatial learning and memory were significantly impaired just in males treated with 1 mg/kg of Ni. With regard to biochemical analysis, activity of catalase (CAT) and superoxide dismutase (SOD) were significantly decreased, while the levels of nitric oxide (NO) and lipid peroxidation (LPO) in the hippocampus were significantly increased in the Ni-treated groups. Consequently, chronic Ni administration induced behavioral and biochemical dysfunctions.

Protective effects of camel milk and vitamin E against monosodium glutamate induced biochemical and testicular dysfunctions

Objective: The current study was outlined to examine the protective effects of camel milk (CM) against the deleterious effects induced by monosodium glutamate (MSG). Methods: MSG was administered either alone or in combination with camel milk or vitamin E for 4 weeks. Serum and testicular tissues were examined using semiquantitative RT-PCR analysis. Results: CM normalized the decrease in serum levels of testosterone, luteinizing hormone (LH), sperm profiles and testicular antioxidant activities that were decreased by MSG. At the molecular levels, MSG down-regulated the mRNA expression of steroidogenesis related genes and receptors of androgen, LH and follicle stimulating hormone. MSG induced testicular apoptosis. All altered genes were normalized and upregulated in presence of CM when compared to the effect of Vit. E. Conclusions: The usage of camel milk as a therapy against MSG used in food industry is very indicative and protective.

Impact of gasoline on health. An updated review on gasoline-induced histopathological effects in laboratory animals

Gasoline was described to induce many biochemical and physiological dysfunctions with subsequent disturbance of health and development of many diseases. It was reported to induce health hazards through generating reactive oxygen species with subsequent harmful effects on the normal body physiology. This work reviewed the previous experimental studies conducted on animal models and aimed to assess the effect of exposure to gasoline through different routes on the different body systems and organs. The histopathological impact of gasoline on the nervous, respiratory, reproductive and immune system was reviewed. Adding to that the impact of exposure to gasoline on the skin, liver, kidneys, blood, bone marrow and genes was also reviewed. It is hoped that this review will encourage and support the conduction of more rigorous studies aimed to assess the impact of gasoline on the health and possibly help optimizing the exposure standards for gasoline and other hydrocarbon fuels.