Accurate forecasting of waste is essential for effective management and allocation of resources. As urban populations grow, the demand for municipal waste systems increases, creating the need for reliable forecasting methods to support planning and decision making. This study compares statistical models Error Trend Seasonality (ETS) and Auto Regressive Integrated Moving Average (ARIMA) with advanced machine learning approaches, including Random Forest (RF), Extreme Gradient Boosting (XGBoost), and Long Short-Term Memory (LSTM) networks. Five waste categories were analyzed: dead animal, building, commercial, domestic, and liquid waste. Historical datasets were used for model training and validation, with accuracy assessed through mean absolute error and root mean squared error. Results indicate that ARIMA generally outperforms ETS in forecasting building, commercial, and domestic waste streams, especially in capturing long-term domestic waste patterns. Both statistical models, however, show limitations in predicting liquid waste due to its irregular and highly variable nature, where even baseline models sometimes perform competitively. In contrast, machine learning methods consistently achieve the lowest forecasting errors across all categories. Their capacity to capture nonlinear relationships and adapt to complex datasets highlights their reliability for real-world waste management. The findings underline the importance of selecting forecasting techniques tailored to the characteristics of each waste type rather than applying a uniform method. By improving forecasting accuracy, municipalities and policymakers can design more effective waste management strategies that align with Sustainable Development Goal 11 on sustainable cities and communities, Sustainable Development Goal 12 on responsible consumption and production, and Sustainable Development Goal 13 on climate action.

Methotrexate (MTX) is a widely used chemotherapeutic and immunosuppressive agent, but its clinical utility is limited by oxidative stress-mediated renal toxicity. This study evaluated the nephroprotective potential of the dietary polyphenolic bioactive molecule piceatannol (PIC) in its crude and liposomal nanoparticle (PIC-LNP) forms against MTX-induced kidney injury in rats. Sixty rats were allocated into six groups and received vehicle, PIC, PIC-LNPs, MTX, or combinations of MTX with PIC or PIC-LNPs. MTX administration induced marked renal dysfunction and oxidative/nitrosative stress, reflected by elevated serum urea, creatinine, and uric acid, together with increased renal ROS, MDA, protein carbonyls, 8-OHdG, and nitric oxide, in parallel with suppression of the Nrf2/HO-1 antioxidant pathway. These disturbances were accompanied by activation of TLR4/NF-κB and MAPK signaling, upregulation of pro-inflammatory cytokines, and a shift toward apoptosis, as evidenced by increased Bax and caspase-3 and reduced Bcl-2 expression. Histological and ultrastructural analyses confirmed extensive glomerular and tubular damage with mitochondrial disruption and cytoplasmic vacuolations. PIC treatment attenuated these MTX-induced alterations, whereas the liposomal formulation conferred superior protection. PIC-LNPs restored Nrf2/HO-1 signaling, enhanced endogenous antioxidant defenses, reduced oxidative/nitrosative and inflammatory responses, and normalized apoptotic markers, accompanied by substantial preservation of renal architecture and cellular integrity. Immunohistochemistry demonstrated strong Nrf2 expression with minimal NF-κB activation in the PIC-LNP group. Collectively, these findings highlight liposomal piceatannol as a promising bioactive-molecule-based strategy for controlling oxidative stress and mitigating chemotherapy-associated oxidative-stress-related renal injury.

Background/Objectives: Arsenic (ARS) exposure is a major cause of kidney injury, driven by oxidative stress, inflammation, fibrosis, and apoptosis. This study evaluated the renoprotective effects of morin (MOR) and morin-loaded PLGA nanoparticles (MOR–PGNPs) against ARS-induced nephrotoxicity in rats. Methods: Sixty male Sprague Dawley rats were randomly allocated into six groups (n = 10 per group). The control group received corn oil. The MOR group received MOR (100 mg/kg), and the MOR–PGNPs group received the same dose of MOR encapsulated in PLGA nanoparticles. ARS was administered at 10 mg/kg for 14 days. Co-treated groups received ARS together with either MOR or MOR–PGNPs, with a 28 min interval between administrations. Renal function markers (serum urea, creatinine, uric acid, renal KIM-1), oxidative stress and antioxidant parameters (Nrf2/HO-1, CAT, SOD, GPx, ROS, MDA), inflammatory mediators (TLR4/NF-κB, TNF-α, IL-6, IL-1β), fibrotic markers (TGF-β1, fibronectin), and apoptotic proteins (caspase-3, caspase-8, Bax, Bcl-2) were assessed, alongside histopathological and ultrastructural evaluations. Results: ARS exposure significantly impaired renal function, increased KIM-1, suppressed Nrf2/HO-1 signaling, reduced antioxidant enzyme activities, and elevated ROS and MDA levels. It also activated TLR4/NF-κB signaling, upregulated pro-inflammatory cytokines and fibrotic markers, and increased pro-apoptotic proteins while downregulating Bcl-2. MOR co-treatment partially ameliorated these alterations. MOR–PGNPs produced potentially enhanced protection, restoring kidney function markers, enhancing antioxidant defenses, and markedly attenuating inflammation, fibrosis, and apoptosis. Histopathological and ultrastructural analyses confirmed preservation of glomerular and tubular architecture, mitochondrial integrity, and minimal cytoplasmic vacuolization in the MOR–PGNPs group. Conclusions: MOR–PGNPs at 100 mg/kg effectively mitigated ARS-induced renal damage through antioxidant, anti-inflammatory, antifibrotic, and anti-apoptotic mechanisms, supporting PLGA-based morin nanoparticles as a promising and safe renoprotective strategy.

Methotrexate (MTX) is widely used for its chemotherapeutic and immunosuppressive properties, but is limited by oxidative stress-mediated hepatotoxicity. Nanoantioxidant delivery systems can enhance the stability, solubility, and in vivo efficacy of natural antioxidants. This study investigated the hepatoprotective effects of myricetin (MYR), a flavonoid with potent antioxidant activity, and its liposomal nanoantioxidant formulation (MYR-loaded liposomal nanoparticles, MYR-LNPs) against MTX-induced liver injury in male albino Sprague Dawley rats. Sixty rats were randomly allocated to six groups: control, MTX, MYR, MYR-LNPs, and combinations of MTX with MYR-LNPs. MYR-LNPs were successfully formulated and physicochemically characterized, exhibiting a mean particle size of 95.6 nm, a zeta potential of −32 mV, and a narrow polydispersity index, collectively confirming their colloidal stability and suitability for hepatic delivery. MTX markedly disrupted liver function, increasing serum AST, ALT, ALP, and bilirubin and decreasing total protein, albumin, and globulin, whereas co-treatment with MYR-LNPs substantially restored these parameters and outperformed free MYR. MTX-induced oxidative stress, reflected by depleted hepatic GSH and antioxidant enzymes (GPx, SOD, CAT, GST), elevated reactive oxygen species (ROS), malondialdehyde (MDA), and protein carbonyls and downregulated NRF2/HO-1, was significantly counteracted by MYR-LNPs. In addition, MYR-LNPs mitigated MTX-evoked inflammation and nitrosative stress by reducing NF-κB, TNF-α, IL-1β, nitric oxide, and iNOS expression. They corrected apoptotic imbalance by lowering Bax and caspase 3 while increasing Bcl-2. Histopathological and ultrastructural assessments confirmed that MYR-LNPs preserved hepatic architecture and mitochondrial integrity. These findings indicate that MYR-loaded liposomal nanoantioxidants provide superior protection against MTX-induced hepatotoxicity by modulating oxidative stress, inflammation, and apoptosis, supporting their potential as an advanced nanodrug delivery strategy for antioxidant therapy.

Background: Cisplatin is a widely used chemotherapeutic agent whose gonadotoxic effects, largely driven by oxidative stress and inflammation, pose a major threat to male reproductive health. This study evaluated whether hesperetin (HES) and hesperetin-loaded poly (lactic-co-glycolic acid) nanoparticles (HES-PLGA-NPs) can protect against cisplatin-induced testicular dysfunction in adult male Sprague Dawley rats. Methods: Sixty rats were randomly assigned to six groups: control, HES, HES-PLGA-NPs, cisplatin (CIS), CIS + HES, and CIS + HES-PLGA-NPs. CIS (7.5 mg/kg/week, i.p.) was given intraperitoneally for four weeks, while HES and nano-HES (50 mg/kg/day, p.o.) were orally administered concurrently. Reproductive hormones, testicular weight, sperm parameters, oxidative stress and antioxidant markers, NRF2/HO-1 and NF-κB signaling, apoptotic indices, ferroptosis-related markers, histopathology, and GPX4/ACSL4 immunoexpression were assessed. Results: CIS caused marked reproductive dysfunction, including reduced testosterone, FSH, and LH, decreased testicular weight, and impaired sperm quality. These changes were associated with severe oxidative and nitrosative stress (↑ MDA, NO, 8-OHdG), depletion of antioxidant defenses (↓ SOD, CAT, GSH), reduced NRF2/HO-1, elevated NF-κB activity and pro-inflammatory cytokines, apoptosis-related changes (↑ Bax, caspase-3; ↓ Bcl-2), and ferroptosis-associated alterations (↑ Fe²⁺, TFR1, lipid ROS, ACSL4, 4-HNE; ↓ GPX4, SLC7A11). Both HES and HES-PLGA-NPs were associated with significant amelioration of these alterations, but the nanoformulation showed more pronounced protection, normalizing several oxidative and ferroptosis-associated markers toward control levels and more effectively preserving seminiferous tubule architecture and spermatogenesis. Conclusions: HES-PLGA-NPs were associated with multi-mechanistic protection against cisplatin-induced oxidative, inflammatory, apoptotic, and ferroptosis-associated damage in the testes, and may represent a promising nanoantioxidant candidate warranting further investigation for preserving male reproductive function during chemotherapy.

Cadmium (Cd) is an environmentally pervasive toxic metal that accumulates in the kidney and promotes oxidative stress, inflammation, and apoptosis. This study evaluated the renoprotective effects of free pterostilbene (PTS) and PLGA-encapsulated PTS (PTS-PLGA) in male Sprague–Dawley rats with Cd-induced nephrotoxicity. Rats received CdCl₂ (2 mg/kg/day, intraperitoneally) for 3 weeks and oral free PTS or PTS-PLGA at a nominal PTS-equivalent dose of 50 mg/kg/day. The formulation dose was calculated from encapsulation efficiency; however, systemic and renal PTS exposure were not measured. Renal function, kidney injury molecule-1 (Kim-1), oxidative stress, inflammatory, and apoptosis-related markers were assessed together with histopathological, ultrastructural, and immunohistochemical changes. Cd exposure impaired renal function and increased Kim-1, reactive oxygen species, malondialdehyde, protein carbonyls, 8-hydroxy-2′-deoxyguanosine, inflammatory mediators, caspase activities, Bax/Bcl-2 ratio, and p53 expression. These changes were accompanied by reduced antioxidant defenses and Nrf2/HO-1-related markers, as well as marked histological and ultrastructural injury. Both PTS formulations attenuated Cd-associated renal alterations. Under the present dosing conditions, PTS-PLGA was associated with greater improvement than free PTS across most endpoints. PLGA-encapsulated PTS therefore warrants further preclinical investigation as a potential approach to mitigate Cd-induced nephrotoxicity; pharmacokinetic, biodistribution, and empty-carrier control studies are needed to define the basis of the observed formulation-related differences.