Sequentially optimized process towards sustainable synthesis of activated carbon from wild thornbush for 4-nitrophenol and industrial effluent treatment.

Environmental nuisance thornbush Prosopis juliflora was utilized as an inexpensive and renewable biomass raw material for the sustainable production of activated carbon. Previously, the sequential muffle furnace-microwave arrangement was effective with acid activation for activated carbon synthesis. However, the intermediate synthesis steps were not optimized. In this work, we have optimized the intermediate steps, viz. chemical impregnation, carbonization, and microwave activation. Sequential optimization for base activation was developed and compared with acid activation. The base-activated carbon (BAC) exhibited a more crystalline nature and faster uptake kinetics than AAC. BAC demonstrated an adsorption capacity of 576 mg/g for 4-nitrophenol (4-NP) surpassing that of optimized acid-activated carbon (AAC) by 45%. The optimal base activation required 1.85 times lower microwave energy than that of the acid activation. BAC exhibited significantly higher BET surface area (1319 m2/g) and micropore volume (0.524 cm3/g) which were about 28% and 26% higher than those of AAC. When compared to biochar obtained from the same thornbush, the BAC exhibited an 11-fold increase in adsorption capacity. The adsorbents could be easily regenerated with ethanol and used up to five cycles. Adsorption using BAC also could achieve 80% COD removal for industrial wastewater, while AAC led to 61% removal. Continuous packed column with BAC revealed a breakthrough time of 3.5 h for industrial effluent while for 500 mg/L 4-nitrophenol, it was 25 h. Prosopis juliflora thornbush, an environmental nuisance, could be converted into a high-capacity adsorbent for environmental remediation after careful sequencing and optimization of the intermediate synthesis steps.

Energy-saving COVID-19 biomedical plastic waste treatment using the thermal - Catalytic pyrolysis.

The rate of Biomedical waste generation increases exponentially during infectious diseases, such as the SARS-CoV-2 virus, which burst in December 2019 and spread worldwide in a very short time, causing over 6 M casualties worldwide till May 2022. As per the WHO guidelines, the facemask has been used by every person to prevent the infection of the SARS-CoV-2 virus and discarded as biomedical waste. In the present work, a 3-ply facemask was chosen to be treated using the solvent, which was extracted from the different types of waste plastics through the thermal-catalytic pyrolysis process using a novel catalyst. The facemask was dispersed in the solvent in a heating process, followed by dissolution and precipitation of the facemask in the solvent and by filtration of the solid facemask residue out of the solvent. The effect of peak temperature, heating rate, and type of solvent is observed experimentally, and it found that the facemask was dissolved completely with a clear supernate in the solvent extracted from the (polypropylene + poly-ethylene) plastic also saved energy, while the solvent from ABS plastic was not capable to dissolute the facemask. The potential of the presented approach on the global level is also examined.

Therapeutic Potential and Pharmaceutical Development of a Multitargeted Flavonoid Phloretin.

Phloretin is a flavonoid of the dihydrogen chalcone class, present abundantly in apples and strawberries. The beneficial effects of phloretin are mainly associated with its potent antioxidant properties. Phloretin modulates several signaling pathways and molecular mechanisms to exhibit therapeutic benefits against various diseases including cancers, diabetes, liver injury, kidney injury, encephalomyelitis, ulcerative colitis, asthma, arthritis, and cognitive impairment. It ameliorates the complications associated with diabetes such as cardiomyopathy, hypertension, depression, memory impairment, delayed wound healing, and peripheral neuropathy. It is effective against various microbial infections including Salmonella typhimurium, Listeria monocytogenes, Mycobacterium tuberculosis, Escherichia coli, Candida albicans and methicillin-resistant Staphylococcus aureus. Considering the therapeutic benefits, it generated interest for the pharmaceutical development. However, poor oral bioavailability is the major drawback. Therefore, efforts have been undertaken to enhance its bioavailability by modifying physicochemical properties and molecular structure, and developing nanoformulations. In the present review, we discussed the pharmacological actions, underlying mechanisms and molecular targets of phloretin. Moreover, the review provides insights into physicochemical and pharmacokinetic characteristics, and approaches to promote the pharmaceutical development of phloretin for its therapeutic applications in the future. Although convincing experimental data are reported, human studies are not available. In order to ascertain its safety, further preclinical studies are needed to encourage its pharmaceutical and clinical development.

Topical Administration of ACE Inhibitor Interrupts the Progression of Cataract in Two Kidney One Clip Induced Hypertensive Cataract Model.

PURPOSE: Previously, we assessed that hypertension increases cataractogenesis. In the present study, we evaluated the effect of oral and topical administration of enalapril on two kidney one clip (2K1C)-induced hypertensive cataract model by evaluating the biochemical alteration of lenticular antioxidants, ionic content, ATPase activity, protein content and careful examination of the lenticular opacity. MATERIALS AND METHOD: Animals were divided into normal and hypertensive animals. Hypertensive animals were divided into hypertensive control group (0.3% CMC), enalapril (oral) treatment group (20 mg/kg/day; p.o), and enalapril (topical) treatment group (0.1% w/v on the eye cornea) for a period of twelve weeks. During experimental study blood pressure, heart rate and morphology of the eyes were monitored biweekly. After twelve weeks, lenses were photographed and various catractogenic biochemical parameters were assessed. RESULTS: Enalapril (oral) treatment conserved the blood pressure (systolic and diastolic), restored the level of antioxidants, restored the lipid peroxidation marker, nitrite content, ionic content, ATPase function, protein content, and thus delayed the cataract formation. While, enalapril (topical) treatment exhibited anti-cataract effect without affecting the systolic and diastolic blood pressure that could be by restoring the antioxidant level, maintaining the ionic balance, balancing the protein levels, and by inhibiting the upregulated ocular renin angiotensin system. The overall results suggest that enalapril (topical) treatment showed conspicuous effect than enalapril (oral) treatment in adjourning the cataract formation. CONCLUSION: Based on the results, it may be concluded that upregulated ocular RAS by increasing oxidative stress and by misbalancing the lenticular ionic and protein content may lead to cataract formation in hypertensive condition.

Role of the renin-angiotensin system in the development of cataract formation in angiotensin-II-induced experimental rats.

Previously, we established several facts regarding hypertension-associated cataractogenesis. As a follow-on study, we evaluated the role of the renin-angiotensin system (RAS) in angiotensin-II (Ang-II)-induced cataract formation in experimental hypertensive rats. Sprague-Dawley male albino rats (150-180 g) were used for the present experiment. The animals were divided into four groups, with six animals in each group. During the 12 weeks of the experimental protocol, the normal group received sterile water (1 ml/kg/day, subcutaneously (sc), and the Ang-II control group received angiotensin (1 mg/kg/day) subcutaneously. The ARB (O) group received olmesartan (2 mg/kg/day) orally, and the ARB (T) group received two drops of olmesartan (5 mM) topically on the cornea; concurrently, both groups were treated with Ang-II (1 mg/kg/day, sc) to induce hypertension. Biweekly, the systolic and the diastolic blood pressures were recorded, and the eyes were examined; moreover, cataractogenic parameters, such as oxidative stress markers and protein contents in the lenses, were evaluated after completion of the experimental protocol. Twelve weeks of olmesartan administered, orally or topically, significantly reduced the progression of cataract formation and restored antioxidants, lipid peroxidation, nitrite content, and protein contents in the lenses of the mice in groups O and T, respectively, as compared with those in the Ang-II control group. On the basis of our results, we conclude that the ocular RAS exacerbates the lenticular oxidative stress that may lead to cataract formation. The results showed that the RAS has an independent and important role in cataract formation under hypertensive conditions.

Therapeutic effects of various renin angiotensin modulators on hyperglycemia-induced cataract formation in Sprague Dawley rats.

OBJECTS: Our previous research work reported the beneficial effects of angiotensin receptor blockers (ARBs) for the treatment of diabetes associated cataract which was induced by streptozotocin (STZ). The current study, evaluated the effects of topical administration of various renin angiotensin modulators on STZ-induced cataracts in rats. METHODS: Single dose of STZ (60 mg/kg, i.p.) was administered in the rats to induce diabetes. Animals were divided into normal and diabetic rats. Normal rats were administered with single dose of sodium citrate buffer (0.1 M, 10ml/kg, i.p.). Diabetic animals were divided into various treatment groups, each group contains six animals and received aliskiren, olmesartan, enalapril, and angiotensin 1-7 at a dose of 0.5% w/v topically on the cornea of the eye for a period of 8 weeks. During experimental protocol morphology of the eyes and lenticular opacity were monitored. Animals were sacrificed after 8 weeks of drug treatment, and various cataractogenic biochemical parameters were assessed. RESULTS: Topical administrations with aliskiren, enalapril, olmesartan, and angiotensin 1-7 showed non-significant alterations in the blood glucose level, but significantly decreased lenticular opacity, restored antioxidant level, restored MDA level and Nitrite content, and decreased the onset of cataract formation. CONCLUSION: Overall, our findings suggest that topical treatment with renin angiotensin modulators delayed the onset of diabetes-induced cataract formation.

Effects of a novel isoflavonoid from the stem bark of Alstonia scholaris against fructose-induced experimental cataract.

OBJECTIVE: The present study investigated the anticataract activity of a novel isoflavonoid, isolated from stem bark of Alstonia scholaris, against fructose-induced experimental cataract. METHODS: The bioactivity of fractions extracted from A. scholaris, an isolated isoflavonoid (ASII) was screened using in vitro (goat lens) and in vivo (albino rats) experimental cataract models. For the in vivo evaluation, albino rats (12-15 weeks old) were divided into five groups (n = 6). Group I (normal) received 0.3% carboxymethyl cellulose solution (10 mL/[kg·d], p.o.). Group II (control) received 10% (w/v) fructose solution in their drinking water. Groups III-V received ASII at three different doses, 0.1, 1.0 and 10 mg/(kg·d), concurrently with 10% (w/v) fructose solution. Treatment was given daily for 8 consecutive weeks. During the protocol, systolic blood pressure, diastolic blood pressure, blood glucose level and lenticular opacity were monitored at 2-week intervals. Pathophysiological markers (catalase, superoxide dismutase, glutathione peroxidase, reduced glutathione and malondialdehyde) in eye lenses were examined at the end of the 8-week treatment period. RESULTS: The results of in vitro study showed that A. scholaris extract and the active fraction (A3) reduced the lenticular opacity as compared to toxic control group. The in vivo study showed that 8-week administration of ASII (0.1, 1.0 and 10 mg/[kg·d], p.o.) led to significant reduction in blood pressure and blood glucose level and retarded the initiation and evolution of cataractogenesis, compared to the fructose-induced cataract model control. Additionally, ASII treatment led to significant improvement in lens antioxidants (catalase, superoxide dismutase, glutathione peroxidase and reduced glutathione) and decreased lens malondialdehyde, compared to the control group (group II). CONCLUSION: Results revealed that administration of ASII played a crucial role in the reduction of cataract formation in diabetic and hypertensive models.

Magnesium taurate attenuates progression of hypertension and cardiotoxicity against cadmium chloride-induced hypertensive albino rats.

The present study was designed to evaluate the antihypertensive activity and cardioprotective effects of magnesium taurate against cadmium chloride (CdCl2)-intoxicated albino rats. Sprague Dawley male albino rats (120-150 g) were divided into five groups having six animals in each group. Hypertension and cardiotoxicity were induced in animals by administration of CdCl2 (0.5 mg/kg/day, i.p.) for four weeks. Magnesium taurate (2 and 4 mg/kg/day) was administered orally after induction of hypertension (after two weeks) in their respective groups concurrently with CdCl2 for next two weeks. Amlodipine (3 mg/kg/day, p.o.) was used as a standard and administered after induction of hypertension. Blood pressure was monitored biweekly by using non-invasive blood pressure system and biochemical parameters and histopathology of the heart were evaluated after four weeks of the experimental protocol. During the four weeks of the experimental protocol, the toxic control group showed significant elevation of systolic and diastolic blood pressure concomitant with augmentation of cardiotoxicity as indicated by reduction in myocardial antioxidants including glutathione peroxidase, catalase, superoxide dismutase, reduced glutathione and increased malondialdehyde level in heart as compared to the normal group. The oral administrations of magnesium taurate significantly restored the blood pressure, myocardial antioxidants and malondialdehyde level as compared to toxic control group. In addition, histopathological examination showed that magnesium taurate treatments substantially reduced the myocardial damages against CdCl2 treatment. The results suggest that magnesium taurate has prominent antihypertensive and cardioprotective activity via its potent antioxidant activity and can be used as a nutrition supplement to improve the cardiovascular health.

Losartan delays the progression of streptozotocin-induced diabetic cataracts in albino rats.

The ocular renin-angiotensin system has become an interesting target for ocular diseases because it has been implicated in various ocular diseases such as diabetic retinopathy, glaucoma, age-related macular degeneration, uveitis, and hypertensive cataracts. In the present study, we explored the effect of topically and orally administered losartan (an angiotensin receptor blocker) on streptozotocin-induced diabetic cataract in albino rats. Topical treatment with losartan modulated neither the blood glucose level nor the polyol content but oral treatment with losartan decreased both. Topical and oral treatment with losartan significantly increased the antioxidants (glutathione, glutathione peroxidase, superoxide dismutase, and catalase), decreased the lipid peroxidant malondialdehyde, and restored soluble protein, and insoluble protein and various ions (Na+ , K+ , and Ca2+ ) in the lens; however, topical treatment had a better effect than oral treatment. These findings demonstrate that topical administration of losartan significantly reduces the risk of cataract formation without affecting either the blood glucose level or polyol contents.

Role of Nitric Oxide in the Development of Cataract Formation in CdCl2-induced Hypertensive Animals.

PURPOSE: Previously we established a strong association of systemic hypertension with cataract formation. In the present study, we investigated the role of nitric oxide (NO) in the development of cataract formation in CdCl2-induced hypertensive animals. MATERIALS AND METHODS: Hypertension was induced in male albino rats by intraperitoneal administration of CdCl2 (0.5 mg/kg/day) for eight weeks. The NO modulators, 10 µM S-nitrosoglutathione (NO donor) and 1% w/v Nω-nitro-L-arginine methyl ester (L-NAME, NOS inhibitor) were applied topically once a day on the eye cornea during the experimental period. Amlodipine (3mg/kg/day) was used as a standard antihypertensive drug and administered orally. RESULTS: In the CdCl2 control group, mean arterial pressure was significantly increased along with augmentation of lens nitrite, opacity, and oxidative stress. The control of hypertension by amlodipine substantially restored lens nitrite and cataractogenic events. Moreover, topical application of L-NAME significantly alleviated the lens nitrite, opacity, antioxidants (GSH, CAT, SOD, and GPx), MDA, proteins, and ionic (Na+ and Ca2+) contents. Whereas, S-nitrosoglutathione topical application exacerbated these cataractogenic events without affecting hypertension as compared to CdCl2 control group. The findings demonstrated that NO donor exacerbates and NOS inhibitor alleviates the cataract formation in hypertensive condition. The control of hypertension also reduces the cataract formation with reduction of lens nitrite level. CONCLUSION: The overall findings suggested the strong correlation between NO and hypertension associated cataract formation. The elevation of lens nitrite (NO metabolite) is one of the key factors of augmentation of lenticular oxidative stress and cataract formation in the hypertensive condition.

Therapeutic targets of renin-angiotensin system in ocular disorders.

PURPOSE: To review current literature on the renin-angiotensin system (RAS)-mediated pathogenic mechanisms and therapeutic targets in ocular diseases. METHODS: A comprehensive literature survey was performed on PubMed, Scopus, and Google Scholar databases published from 1977 to 2016. The search terms were a RAS, angiotensin, angiotensin receptor, prorenin, pro (renin) receptor, angiotensin converting enzyme inhibitor, angiotensin receptor blocker associated with ocular disorders like cataract, glaucoma, diabetic retinopathy (DR), macular degeneration, and uveitis. Articles were reviewed on the basis of the association between ocular disorders and RAS and relevant articles were discussed. RESULTS: The literature revealed that the individual RAS components including renin, angiotensins, angiotensin converting enzymes, and RAS receptors have been expressed in the specific ocular tissues like retina, choroid, and ciliary body. The activation of both circulatory and local RAS potentiate the various inflammatory and angiogenic signaling molecules, including vascular endothelial growth factor (VEGF), extracellular signal-regulated kinase, and advanced glycation end products (AGE) in the ocular tissues and leads to several blinding disorders like DR, glaucoma, and macular degeneration. The classical and newer RAS inhibitors have illustrated protective effects on blinding disorders, including DR, glaucoma, macular degeneration, uveitis, and cataract. CONCLUSIONS: The RAS components are present in the extrarenal tissues including ocular tissue and have an imperative role in the ocular pathophysiology. The clinical studies are needed to show the role of therapeutic modalities targeting RAS in the treatment of different ocular disorders.

Magnesium taurate prevents cataractogenesis via restoration of lenticular oxidative damage and ATPase function in cadmium chloride-induced hypertensive experimental animals.

Previously we found that hypertension potentiates the risk the cataractogenesis. In the present study, we investigated the protective effects of magnesium taurate (MgT) on hypertension and associated lenticular damages against cadmium chloride (CdCl2)-induced hypertensive animals. Male Sprague-Dawley albino rats (150-180g) were assigned to five experimental groups (n=6). Among the five groups, normal group received 0.3% carboxymethyl cellulose (10ml/kg/day, p.o.). Hypertension control group received CdCl2 (0.5mg/kg/day, i.p.). Tests and standard groups received MgT (3 and 6mg/kg/day, p.o.) and amlodipine (3mg/kg/day, p.o.) concurrently with CdCl2 respectively, for six consecutive weeks. Blood pressure, heart rate, and eyes were examined biweekly, and pathophysiological parameters in serum and eye lenses were evaluated after six weeks of the experimental protocol. The chronic administration of MgT concurrently with CdCl2 significantly restored the blood pressure, serum and lens antioxidants (CAT, SOD, GPx, and GSH), MDA level, and ions (Na+, K+, and Ca2+). Additionally, MgT treatment led to significant increase in the lens proteins (total and soluble), Ca2+ ATPase, and Na+K+ ATPase activity as compared to hypertension control group. Ophthalmoscope observations indicated that MgT treatments delayed the progression of cataract against the hypertensive state. The study shows that MgT prevents the progression of cataractogenesis via restoration of blood pressure, lenticular oxidative damages, and lens ATPase functions in the hypertensive state. The results suggest that MgT supplement may play a beneficial role to manage hypertension and associated cataractogenesis.

Olmesartan, an angiotensin II receptor blocker inhibits the progression of cataract formation in cadmium chloride induced hypertensive albino rats.

AIMS: Previously we found that cadmium chloride (CdCl2) exposure substantially elevates hypertension and potentiates cataract formation. In the present study, we investigated the protective effects of olmesartan, an angiotensin II receptor blocker against cataractogenesis in the CdCl2-induced hypertensive animal model. MAIN METHODS: Male Sprague-Dawley albino rats (150-180g) were randomly selected and assigned to four groups (n=6). Among the four groups, one group (normal) received 0.3% carboxymethyl cellulose (10ml/kg/day, p.o.), another group (CdCl2 control) received CdCl2 (0.5mg/kg/day, i.p.), and remaining two groups received olmesartan at two doses level (2 and 4mg/kg/day, p.o.) concurrently with CdCl2 for six consecutive weeks. Blood pressure and cataract formation were examined biweekly, and pathophysiological parameters in serum and eye lenses were evaluated after six weeks of the experimental protocol. KEY FINDINGS: The olmesartan treatment significantly restored the blood pressure, lenticular opacity, serum and lens antioxidants (catalase, superoxide dismutase, glutathione peroxidase, and glutathione reduced), and malondialdehyde level. Additionally, it significantly restored the proteins, ions (Na+, K+, and Ca2+), and ATPase pumps activity (Na+K+ ATPase and Ca2+ ATPase) in the lens as compared to CdCl2 control group. SIGNIFICANCE: The findings demonstrate that olmesartan potentially inhibits the risk of cataract formation in the hypertensive state via restoration of lenticular oxidative stress, ATPase function, and ionic contents in the eye lenses. The results suggest that angiotensin II receptor blockers play an important role to prevent cataract formation in several pathogenic conditions like hypertension, diabetes, and oxidative stress.

Hypertension potentiates cataractogenesis in rat eye through modulation of oxidative stress and electrolyte homeostasis.

PURPOSE: To evaluate modes of cataractogenesis in the hypertensive state by using different hypertensive animal models, including fructose, cadmium chloride (CdCl2), N ω-nitro-l-arginine methyl ester (l-NAME), and two-kidney, one clip (2K1C) method. METHODS: Male Sprague-Dawley albino rats (150-180 g) were divided into different groups, each group containing six animals. Hypertension was induced in animals via six weeks administration of fructose (10% solution in drinking water), CdCl2 (0.5 mg/kg/day, i.p.), and l-NAME (20 mg/kg/day, p.o.) in their respective groups and NaCl (0.9% solution in drinking water) in the 2K1C group. The Ramipril-treated group (2 mg/kg/day, orally) served as a standard group for the 2K1C animal model. Blood pressure was measured biweekly using non-invasive blood pressure system. The biochemical parameters in serum and eye lenses were evaluated after six weeks of the experimental protocol. RESULTS: Hypertensive animal models showed significant induction of systolic and diastolic blood pressure and modulation of oxidative stress through depletion of antioxidants, including glutathione peroxidase, catalase, superoxide dismutase, glutathione, and elevation of malondialdehyde in serum and eye lenses. A significant elevation of ionic contents (Na(+) and Ca(2+)) and reduction of total protein and Ca(2+) ATPase activity in eye lenses were observed in all hypertensive animal models except l-NAME when compared with the normal group. The significant restoration of the antioxidants, Malondialdehyde (MDA) total protein, and ionic contents in the eye lenses concomitant with reduction of blood pressure were observed in the ramipril-treated group as compared to the 2K1C animal model. The results indicate that the fructose, CdCl2, and 2K1C models showed pronounced cataractogenic effects in the rat eye lenses. CONCLUSION: Based on our findings, it can be concluded that systemic hypertension significantly increases the risk of cataract formation in the rat eyes via modulation of the antioxidant defense mechanism and electrolyte homeostasis.

Cinnamaldehyde Attenuates Cataractogenesis via Restoration of Hypertension and Oxidative Stress in Fructose-Fed Hypertensive rats.

OBJECTIVES: Several studies have revealed that systemic hypertension is strongly associated with cataractogenesis. However, the pathophysiology and treatment is often unclear. In this study, we evaluated the anti-cataractogenic effect of cinnamaldehyde (CA), a natural organic compound, in rats with fructose-induced hypertension. METHODS: The rats were divided into six groups. For six weeks, the normal group received a suspension of 0.5% carboxy methyl cellulose (10 mL/kg/day, p.o.) while five other groups received a 10% (w/v) fructose solution in their drinking water to induce hypertension. By the end of the third week hypertension had been induced in all the animals receiving fructose. From the beginning of the fourth week to the end of the sixth week, one of those five groups (control) continued to receive only 10% (w/v) fructose solution, one group (standard) received ramipril (1 mg/kg/day, p.o.) plus 10% (w/v) fructose solution, and three groups (experimental) received CA at doses of 20, 30, and 40 mg/kg/day p.o., plus 10% (w/v) fructose solution. Blood pressure was measured weekly using a non-invasive blood pressure apparatus. After six weeks, the animals were sacrificed, and the anti-cataractogenic effects on the eye lenses were evaluated. RESULTS: Administration of fructose elevated both the systolic and the diastolic blood pressures, which were significantly reduced by CA at all dose levels. In the control group, a significant increase in the malonaldehyde (MDA) level and decreases in the total protein, Ca(2+)adenosine triphosphate (ATP)ase activity, glutathione peroxidase, catalase, superoxide dismutase and glutathione levels, as compared to the normal group, were observed. Administration of CA at all doses significantly restored the enzymatic, non-enzymatic, antioxidants, total protein, and Ca(2+)ATPase levels, but decreased the MDA level, as compared to the control group. CONCLUSION: The present study revealed that CA modulated the antioxidant parameters of the serum and lens homogenates in hypertension-induced cataractogenic animals.

Animal models of erectile dysfunction.

Erectile dysfunction (ED) is a prevalent male sexual dysfunction with profound adverse effects on the physical and the psychosocial health of men and, subsequently, on their partners. The expanded use of various types of rodent models has produced some advances in the study of ED, and neurophysiological studies using various animal models have provided important insights into human sexual dysfunction. At present, animal models play a key role in exploring and screening novel drugs designed to treat ED.