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Bioaccumulation of heavy metals can cause physiological and biochemical alterations in aquatic animals. Accumulation of Cd and Pb and oxidative response in the liver and muscle of fish species; Scatophagus argus, Plotosus lineatus, Netuma thalassina and Mugil cephalus were evaluated. Accumulation of Cd, Pb and oxidative response indicated by malondialdehyde (MDA) were significantly higher in the liver than muscle in all coastal fish species. Antioxidative parameters, such as reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD), varied. S. argus exhibited the highest levels of Cd and Pb accumulation, both in the liver and muscle. Simultaneous activation and depression of oxidative defense mechanism was depicted in S. argus's liver which indicated by positive correlation of Pb to CAT activity and negative correlation of Pb to SOD activity. Positive correlation was significance for Cd and Pb accumulation in the liver and muscle of M. cephalus, which may be used for pollution biomonitoring. The present study indicated the oxidative response to Cd and Pb accumulation was emphasise in liver, while oxidative response varied in each coastal fish species. Accumulation of Cd, Pb, and oxidative status, i.e., lipid peroxidation level indicated by malondialdehyde (MDA), was significantly higher in the liver than muscle in 4 coastal fish species (Scatophagus argus, Plotosus lineatus, Netuma thalassina, and Mugil cephalus). S. argus exhibited the highest levels of Cd and Pb accumulation, both in the liver and muscle, when compared to other three coastal fish species. The liver's oxidative response to Pb was high in S. argus, and represented simultaneous activation and depression of antioxidative defense mechanism. A significant positive correlation was revealed for Cd and Pb accumulation in the liver and muscle of M. cephalus, which may be used for pollution biomonitoring. [ABSTRACT FROM AUTHOR]

Objective: The present study investigated the effects of a local Thai vegetable, Tiliacora triandra (Colebr.) Diels, also known as Yanang, against cerebral ischemia/reperfusion injury in mice. Materials and Methods: Thirty male ICR mice were divided into three experimental groups of BLCCAO + 10% Tween 80, BLCCAO + T. triandra 300 mg/kg, and BLCCAO + T. triandra 600 mg/kg. Cerebral ischemia/reperfusion was induced by three minutes of bilateral common carotid artery occlusion (BLCCAO) followed by 18 days of reperfusion. Leaf extract was administered orally 24 hours after arterial occlusion and continued for 18 consecutive days. Cognitive abilities were evaluated using the Morris water maze. Histological analysis was conducted in the dorsal hippocampus subregions CA1, CA3, and DG and white matter regions (the corpus callosum, internal capsule, and optic tract) using 0.1% cresyl violet and 0.1% Luxol fast blue staining. Results: Results showed that T. triandra leaf extract at the doses of 300 and 600 mg/kg significantly enhanced spatial learning, and learning flexibility, and prevented neuronal death in the DG of mice following ischemia/reperfusion. Conclusion: T. triandra leaf extract enhanced spatial learning, and learning flexibility, and prevented DG neuronal death in a mice model of cerebral ischemia/reperfusion. [ABSTRACT FROM AUTHOR]

Recently, unilateral common carotid artery occlusion (UCO) in rodents has been suggested as a means of elucidating pathomechanisms of vascular dementia (VaD), especially subcortical ischemic vascular dementia (SIVD). Based on the severity of mild chronic cerebral hypoperfusion, the present study aims to investigate the early onset effects of mild chronic cerebral hypoperfusion caused by permanent right common carotid artery occlusion (rCCAO) on the dorsal hippocampal neurons and white matter areas. Thirty male Sprague-Dawley rats were randomly divided into Sham and rCCAO according to histopathology analytical periods of two, four, and eight weeks of rCCAO. Results showed that significant neuronal death in the CA1 region was found at eight weeks of rCCAO. However, rCCAO for two, four, and eight weeks did not induce significant neuronal death in the CA3 and DG regions, and there were no signs of white matter density reduction in the corpus callosum, the internal capsule, or the optic tract. In conclusion, rCCAO for eight weeks significantly induced neuronal death in CA1 but not in the CA3, DG regions or white matter areas. Therefore, the CA1 region was the most susceptible to mild chronic cerebral hypoperfusion induced by permanent right common carotid artery occlusion in male Sprague-Dawley rats. [ABSTRACT FROM AUTHOR]

Background: Momordica charantia (M charantia) seed has been supposed to have an antifertility property but mechanisms underlying the infertility effect have not been investigated. Objective: We investigated the antifertility effect of M. charantia ethanol seed extracts on reproductive toxicology and seminal and plasma testosterone in male Wistar rats. Materials and Methods: The control group (I) was provided daily 1 ml dimethyisulfoxide (DMSO) and the experimental groups II and III were given daily 400 and 800 mg dry matter/kg body weight of the extracts dissolved in 1 ml DMSO via the esophageal route. All groups were administered for 42 days (day 42). Changes in body weight, fertility, reproductive characteristics, testicular histopathology and levels of seminal and plasma testosterone among three groups were compared. Results: On day 42, the extracts caused antifertility (p=0.001). The extracts demonstrated significant reductions in diameters of seminiferous tubules and epididymides, spermatid density, daily sperm production and caudal epididymal spermatozoa, sperm motility and viability (p=0.046). Pathological changes in seminiferous tubules revealed atrophy, desquamation, pyknosis nucleus and multinucleated giant cell. Plasma cells were evident in three parts of epididymides of rats treated with high dose of the extract. Furthermore, the high dose of the extract suppressed seminal testosterone level (p=0.001) and plasma testosterone level (p=0.002). Conclusion: Our data showed that high dose of M. Charantia seed extracts caused infertility in male rats. The interruption in their fertility was probably attributed to the direct toxic to seminiferous tubules, epididymis and the lowered testosterone level which might impact on sperm parameters. [ABSTRACT FROM AUTHOR]

The present study investigated the neural health benefit of beta-sitosterol (BSS) against trimethyltin (TMT)-induced neurodegeneration in mice. Forty male Institute of Cancer Research (ICR) mice were randomly divided into Sham-veh, TMT-veh, TMT-BSS50, and TMT-BSS100. A one-time intraperitoneal injection of 2.6 mg/kg of TMT was given to mice in TMT groups. Vehicle (veh), BSS 50 mg/kg or BSS 100 mg/kg were orally given for 2 weeks. Spatial learning and memory were evaluated. Brain oxidative status, hippocampal neuropathology, and reactive astrocytes were done. White matter pathology was also evaluated. The results indicated the massy effect of TMT on induced motor ability and spatial memory deficits in accordance with increased neuronal degeneration in Cornus ammonis (CA) 1, CA3, and dentate gyrus (DG) and internal capsule white matter damage. TMT also induced the reduction of reactive astrocytes in CA1 and DG. Brain's catalase activity was significantly reduced by TMT, but not in mice with BSS treatments. Both doses of BSS treatment exhibited improvement in motor ability and spatial memory deficits in accordance with the activation of reactive astrocytes in CA1, CA3, and DG. However, they successfully prevented the increase of neuronal degeneration in CA1 found only with the BSS dose of 100 mg/kg, and it was indicated as the effective dose for neuroprotection in the vulnerable brain area. This study demonstrated mitigative effects of BSS against motor ability and memory deficits with neural health benefits, including a protective effect against CA1 neurodegeneration and a nurturing effect on hippocampal reactive astrocytes.

We investigated the neurological effects of the varied erinacine composition of different mycelia cultures in mice with trimethyltin (TMT)-induced neurodegeneration. Forty male ICR mice were randomly divided into five groups of Sham-veh, TMT-veh, TMT-EME, TMT-EMR and TMT-EME/R. The TMT groups received 2.6 mg/kg one-time intraperitoneal injections of TMT. Oral dosages of 200 mg/kg erinacine combination from each Hericium erinaceus mycelia (EM) cultivated formula (100% eucalyptus wood [E], 100% rubber wood [R], or 40% eucalyptus wood/60% rubber wood [E/R]) were given for two weeks. Spatial learning, memory, flexibility, and anxious behaviour were evaluated alongside brain tissues' oxidative status and histological analyses. Erinacine composition from EME/R exhibited significant positive effects on spatial learning, memory, flexibility, and anxiety ( p < 0.05). These findings emerged concurrently with the significant mitigation of hippocampal lipid peroxidation, CA1 hippocampal, cortical neuron, and corpus callosum white matter degeneration ( p < 0.05). These neurological benefits were associated with the EME/R composition of erinacine A, C, D, G, H, I, K and R. The best neuroprotective effect against TMT-induced neurodegeneration in mice is offered by the EME/R erinacine composition according to its anti-lipid peroxidation, its nurturing effect on neuronal and white matter, and mitigation of behavioural deficits., Competing Interests: CONFLICTS OF INTEREST The authors declare that no conflict of interest., (© Penerbit Universiti Sains Malaysia, 2023.)

Objective: The present study investigated possible neuroprotective effects of ethanolic extract of Tiliacora triandra leaf against cerebral ischemic-reperfusion injury in mice., Materials and Methods: Forty male Institute of Cancer Research (ICR) mice were randomly divided into five groups: (1) Sham + 10% Tween 80, (2) bilateral common carotid artery occlusion (BCCAO) + 10% Tween 80, (3) BCCAO + T. triandra 300 mg/kg, (4) BCCAO + T. triandra 600 mg/kg and (5) BCCAO + quercetin 10 mg/kg. Cerebral ischemic-reperfusion (IR) was induced by 30 min of BCCAO followed by 45 min of reperfusion. After IR induction, total brain protein, calcium, malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH), as well as brain infraction and histopathological changes in vulnerable brain areas, such as the cerebral cortex and hippocampus, were evaluated., Results: The results showed that 2 weeks of pretreatment with T. triandra leaf extract at doses of 300 and 600 mg/kg significantly reduced calcium and MDA, but increased GSH and SOD and CAT activities. The extract significantly attenuated brain infarction and neuronal death in the cerebral cortex and hippocampus., Conclusion: We demonstrated the neuroprotective effects of T. triandra leaf extract against cerebral IR injury in mice.