The presence of pharmaceutical emerging contaminants (PECs) in natural waters has drawn the attention of many Scientists worldwide. Reports on the presence of these contaminants in different water systems continue to increase over the last few decades. This provokes worry about their potential negative implications to biodiversity and humans and their accumulation over a long period of time due to their ability to biotransform and thus breaks down into metabolites that can be more bioactive than the drug itself. Additionally, they can potentially create physiological effects in humans at small doses. This research involved preliminary investigations on disposal practices of expired drugs by pharmacists within Kaduna Metropolis. Water and fish samples from river Kaduna were collected and prepared for GCMS analysis to detect the presence of PECs. Preliminary investigations on disposal practices of expired drugs by pharmacists within Kaduna metropolis revealed that about 60% of the pharmacists discard their expired products by either dumping in bin or burning; 20% reported to follow National (NAFDAC) guidelines while about 20% either refused to respond or were not aware about the disposal practices. The GC-MS results obtained for water sample revealed the presence of N-(3-methylbutyl) acetamide (335 g/L), acetic acid (81 g/L) and cyclopentaneundecanoic acid (140 g/L). Whereas in fish sample, 26-nor-5-cholesten-3-beta.-ol-25-one (400 g/kg), 1,3-benzene diol (160 g/kg), cyclopentaneundecanoic acid (170 g/kg) as well as N- (3-methylbutyl) acetamide (40 g/kg) were present. Some of the compounds found in relatively lower concentrations in the water sample were phthalic acid (27 g/L), guanidine (27 g/L), gluconic acid (17 g/L) and silver acetate (0.7 g/L) while in fish sample, hydroxylamine (3 g/kg), 1,5 heptadiene (12 g/kg) and silane (4 g/kg) were present. Most of the compounds detected are either esters, acids and alcoholic compounds. Studies on PECs in Nigeria are either ignored or limited especially in Northern part of the Country despite its occurrence in different locations and different environmental compartments with variations in concentrations. This research will create awareness and expose individuals and stakeholders to the potential negative effects of these contaminants. Pharmaceutical chemicals are very broad which include solvents, water, reactants and others. They are found in different environmental compartments. Many PECs are found in both the water and fish samples. Accumulation of these contaminants over time could be deleterious to life.

Background: Ethanol intake can cause oxidative stress, tissue inflammation, and renal damage by producing free radicals. Flavonoids are phenolic chemicals found in a range of fruits, vegetables, tea, and wine. More significantly, many flavonoids are active constituents in traditional Chinese herbal medicines, which have no adverse effects in general. However, there is a paucity of research on the therapeutic effectiveness of Citrullus lanatus seed flavonoids against renal damage. Method: The rats were split into six groups: normal, ethanol (10 ml/kg of 50% ethanol), flavonoids (100 mg/kg/day), ethanol plus low and high flavonoid dosages (ET + 100 and 200 mg/kg FCL), and ethanol plus Silymarin (ET + 100 mg/kg SLY). The levels of serum urea, creatinine, uric acid, and nitrite oxide (NO) were measured, as were oxidative stress markers such as superoxide dismutase (SOD), catalase (CAT), glutathione (GPx), malondialdehyde (MDA), and inflammatory markers such as tumour necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β). Then, the kidney organ was harvested for histological study. Results: Citrullus lanatus seed flavonoids (FCL) substantially (p < 0.05) reduced ethanol-induced increases in creatinine, urea, and uric acid. When rats administered FCL were compared to untreated ethanol rats, there was a significant increase (p < 0.05) in CAT, SOD, and GPx levels, as well as decreased MDA. FCL significantly reduced IL-1β and TNF-α levels in ethanol-treated rats. A histological examination significantly corroborated the biochemical assay result. Conclusions: The findings of this study show that the flavonoid-rich fraction of Citrullus lanatus seed has therapeutic potential against ethanol-induced kidney injury by lowering the rise in renal function, inflammatory markers, and oxidative stress. As a result, FCL may work as a plant-based natural therapy to minimise kidney damage. As a result, in the preclinical context, FCL has the potential to minimise organ toxicity for oral therapeutic purposes.

Ethanol consumption can generate free radicals and cause oxidative stress, tissue inflammation, and kidney impairment. It has long been known that saponins from natural sources have numerous therapeutic benefits in African herbal and traditional medicine. However, the study aimed to the study aimed to evaluate the ameliorative effect of saponin-rich extract of Citrullus lanatus seed against ethanol-induced kidney injury. Rats were divided into six groups: a normal control, an ethanol control (10 ml/kg of 50

Dyslipidemia, diabetes, and the upregulation of receptors for oxidized low-density lipoprotein all contribute to hepatic and aortic endothelial dysfunction. The current research examined how camel milk could possibly decrease induced Streptozotocin-high fat diet-aggravated dyslipidemia-mediated damage in male pig hepatic and aortic tissues. Twenty-five pigs were separated into five groups of five pigs each, with five non-atherosclerotic pigs in the control group and twenty atherosclerotic pigs in the experimental groups. Groups 1 and 2 received distilled water as the standard control and atherosclerotic control groups, respectively, while Groups 3 and 4 received camel milk at 250 mL/day and 500 mL/day, respectively, and Group 5 received Metformin at 500 mg/day. The experiment lasted ten weeks. After 10 weeks, all of the pigs were euthanized. The lipid profile and liver enzyme levels were determined from the analysis of blood serum and the histology of the liver and aortic. When pigs administered, camel milk were compared to atherosclerotic control pigs, there was a significant decrease (p 0.05) in cholesterol, triglyceride, low density lipoprotein (LDL), and very low-density lipoprotein (VLDL) levels, while a significant increase in high density lipoprotein levels was observed in pigs that received camel milk. Also, pigs in groups that received camel milk had their liver enzyme parameters (ALP, AST, ALT, GGT, LDH, and CK-MB) significantly lowered when compared with atherosclerotic control pigs. Similarly, treatment with camel milk ameliorates aortic tissues from degradation and reduces histological liver steatosis, and it also decreases the expression of LOX-1 mRNA in the aorta of atherosclerotic pigs.

The purpose of the study was to determine how camel milk affects hyperglycemia, beta-cell function, oxidative stress, and inflammatory markers in type 2 diabetic pigs. Twenty-five (25) pigs were separated into five (5) groups of five pigs each, with five (5) non-diabetic and twenty (20) diabetic pigs in each group. Groups 1 and 2 received distilled water as the standard control and diabetic control groups, respectively, while Groups 3 and 4 received camel milk at 250 mL/day and 500 mL/day, respectively, and Group 5 received metformin at 500 mg/day. The experiment lasted ten weeks. At the end of the ten weeks, all the pigs were euthanized. Treatments with camel milk substantially enhance glucose fasting levels by reducing hyperglycemia in diabetic pigs, significant level at (p < 0.05). When pigs given camel milk were compared with untreated diabetic pigs, there was a substantial rise (p < 0.05) in superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH) levels. Also, camel milk substantially lowered the levels of interleukin (IL-1β) and tumour necrosis factor-alpha (TNF-α) in diabetic pig serum. Similarly, immunohistochemical analysis of islet cells revealed an increase in insulin production, implying improved glycemic control and the eventual commitment of glucose to glycolysis. The bioactive-mediated anti-hyperglycemic and insulin release potential of camel milk treatments contributed to improving type 2 diabetes mellitus. Camel milk improved beta-cell function while reducing oxidative stress and inflammation in type 2 diabetic pigs.