Cisplatin is a chemotherapeutic agent widely used in treatment of several cancers. It is documented as a major cause of clinical nephrotoxicity and hepatotoxicity. The purpose of this study was to investigate the involvement of oxidative stress in the pathogenesis of cisplatin-induced liver and kidney injury. Wistar rats were divided into four groups. Group 1 (control) was intraperitoneally (IP) injected with a single dose of 0.85% normal saline. Groups 2, 3 and 4 were IP injected with single doses of cisplatin at 10, 25 and 50 mg/kg body weight (BW), respectively. At 24, 48, 72, 96 and 120 h after injection, BW, levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), creatinine, malondialdehyde (MDA), and activity of superoxide dismutase (SOD) and histology of the liver and kidney were evaluated. Cisplatin caused a reduction in BW of rats in groups 2, 3 and 4 at all post injection intervals. The levels of serum ALT, AST, BUN and creatinine and MDA of the kidney and liver were markedly increased especially at 48 and 72 h, whereas the activity of SOD was decreased after cisplatin injection. Liver sections revealed moderate to severe congestion with dilation of the hepatic artery, portal vein and bile duct and disorganization of hepatic cords at 50 mg/kg of cisplatin. Kidney sections illustrated mild to moderate tubular necrosis at 25 and 50 mg/kg of cisplatin. Therefore, oxidative stress was implicated in the pathogenesis of liver and kidney injury causing biochemical and histological alterations.

Backgroundcis-Diammineplatinum (II) dichloride (cisplatin) is the important anti-cancer agent useful in treatment of various cancers. Unfortunately, it can produce unwanted side effects in various tissues, including the liver. The present study investigated the possible protective role of curcumin and α-tocopherol against oxidative stress-induced hepatotoxicity in rats upon cisplatin treatment.MethodsMale Wistar rats were divided into five groups (n = 5). Saline and Cis groups, rats were intraperitoneal (i.p.) injected with normal saline and cisplatin [20 mg/kg body weight (b.w.)], respectively. Cis + α-tocopherol group, Cis + Cur group and Cis + α-tocopherol + Cur group, rats were pre-treated with a single dose of α-tocopherol (250 mg/kg b.w.), curcumin (200 mg/kg b.w.) and combined α-tocopherol with curcumin, respectively, for 24 h prior the administration of cisplatin. After 72 h of first injection, specimens were collected. Liver enzyme, lipid peroxidation biomarker, liver histopathology and gene expression of liver nicotinamide adenine dinucleotide phosphate (NADPH) oxidase were investigated.ResultsCisplatin revealed a significant increase of hepatic malondialdehyde (MDA) levels and a significant reduction of hepatic superoxide dismutase (SOD) and catalase activities compared to the saline group. It elicited a marked increase of the serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels and demonstrated the liver pathologies including liver congestion, disorganization of hepatic cords and ground glass appearance of hepatocytes. It also demonstrated a significant increase of NADPH oxidase gene expression compared to saline group. Pre-treatment with combined curcumin and α-tocopherol improved the liver enzymes, lipid peroxidation biomarker, liver histopathology and gene expression of liver NADPH oxidase in cisplatin-treated rats.ConclusionsThe findings indicate that pre-treatment with combined curcumin and α-tocopherol can protect cisplatin-induced hepatotoxicity including the biochemical, histological and molecular aspects. The down-regulations of NADPH oxidase gene expression may be involved in abrogating oxidative stress via reduction of reactive oxygen species (ROS) production.

Acute kidney injury (AKI) is the common clinical syndrome which is associated with increased morbidity and mortality. The severity extends from less to more advanced spectrums which link to biological, physical and chemical agents. Oxidative stress (OS)-related AKI has demonstrated the increasing of reactive oxygen species (ROS) and reactive nitrogen species (RNS) and the decreasing of endogenous antioxidants. Medicinal plants-derived antioxidants can be ameliorated oxidative stress-related AKI through reduction of lipid peroxidation (LPO) and enhancement of activities and levels of endogenous antioxidants. Therefore, medicinal plants are good sources of exogenous antioxidants which might be considered the important remedies to ameliorate pathological alterations in oxidative stress-related AKI.

BackgroundSoil-transmitted helminth (STH) infections are among the most common type of infections worldwide and are widely distributed in tropical areas. In rural areas of southern Thailand where most land is used for agriculture, children are at risk of acquiring parasites, especially STHs. Assessing the current situation regarding parasitic infection in these areas is a prerequisite for developing appropriate control measures. This study is aimed at determining the prevalence of intestinal parasitic infections, the intensity of STH infections and the associated risk factors among primary schoolchildren in Nopphitam District, Nakhon Si Thammarat Province, Thailand.MethodsA cross-sectional study involving 299 schoolchildren between 7 and 12 years of age was conducted between January and March 2016. A questionnaire administered by direct interviews was used to collect sociodemographic information and data on associated risk factors. Stool samples were processed using direct wet smears, formalin-ethyl acetate sedimentation concentration, and the modified Kato-Katz technique.ResultsThe overall prevalence of intestinal parasites among the 299 children was 16% (48 of 299), with 32 children infected with hookworms (10.7%), 10 with Blastocystis hominis (3.3%), seven with Giardia intestinalis (1.6%), one with Enterobius vermicularis (0.3%), and one with Trichuris trichiura (0.3%). The hookworm infection intensity, measured by the median eggs per gram (EPG) of stool, was 1200 EPG (Interquartile range (IQR): 360–3200). Most children had light-intensity hookworm infections, but two had heavy-intensity infections. When participants included in the sample were classified by age, children 10–12 years old demonstrated higher intestinal parasite prevalence than those aged 7–9 years (adjusted odds ratio (AOR) = 2.3, 95% CI: 1.1–4.9, P = 0.030). Inadequate handwashing before meals was statistically associated with hookworm infections (AOR = 2.3; 95% CI: 1.1–4.8, P = 0.037).ConclusionsThis study highlights that hookworms are the most prevalent STH infection in the study area. Older age group (10–12 years) and inadequate handwashing before meals were statistically associated with hookworm infections. Accordingly, appropriate strategies and education on personal and environmental hygiene should be implemented. Moreover, the cost-effectiveness of mass drug administration in this area should be further investigated.Electronic supplementary materialThe online version of this article (10.1186/s12889-018-6023-3) contains supplementary material, which is available to authorized users.

Essential oils are volatile fragrance liquids extracted from plants, and their compound annual growth rate is expected to expand to 8.6% from 2019 to 2025, according to Grand View Research. Essential oils have several domains of application, such as in the food and beverage industry, in cosmetics, as well as for medicinal use. In this study, Michelia alba essential oil was extracted from leaves and was rich in linalool components as found in lavender and jasmine oil. The effects of inhaling michelia oil on human brainwaves still need to be elucidated. Ten male and ten female subjects were recruited. Thirty-two-channel electroencephalography was recorded. The raw data were spectrally analyzed for slow alpha, fast alpha, low beta, mid beta, and high beta activities. The results demonstrate that michelia leaf oil could reduce the alertness level observed by beta wave decrease and fast alpha wave activity increase. The inhalation of pure linalool showed virtually identical responses as the michelia oil inhalation. In conclusion, the sedative effects of michelia oil inhalation might originate from its major linalool component.

Currently, oxidative stress (OS) has become a major interest in point of basic science and clinical research. The imbalance between generations and clearances of oxidants leads to OS. Oxidants are mainly composed of reactive oxygen species (ROS) and reactive nitrogen species (RNS) which are manifested as oxidized macromolecules causing deleterious effects in several organs. Lipid, protein and DNA oxidation products can provide extensively approach of potential oxidative stress biomarkers. OS leads to the fundamental cellular and tissue damages and consequence effect to various organs or systems. This review emphasizes the systemic pathology induced by OS that particularly affect to specialized organs or systems including the nervous system, the cardiovascular system, the lung, the liver and the kidney.

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Ceftriaxone (CTX) exerts a neuroprotective effect by decreasing glutamate excitotoxicity. We further studied the underlying mechanisms and effects of CTX early post-treatment on behavior in a cerebral hypoperfusion rats. The rats’ common carotid arteries (2VO) were permanently ligated. CTX was treated after ischemia. Biochemical studies were performed to assess antioxidative stress and inflammation. Behavioral and histological studies were then tested on the ninth week after vessel ligation. The 2VO rats showed learning and memory deficits as well as working memory impairments without any motor weakness. The treatment with CTX was found to attenuate white matter damage, MDA production, and interleukin 1 beta and tumor necrosis factor alpha production, mainly in the hippocampal area. Moreover, CTX treatment could increase the expression of glia and the glial glutamate transporters, and the neuronal glutamate transporter. Taken together, our data indicate the neuroprotective mechanisms of CTX involving the upregulation of glutamate transporters’ expression. This increased expression contributes to a reduction in glutamate excitotoxicity and oxidative stress as well as pro-inflammatory cytokine production, thus resulting in the protection of neurons and tissue from further damage. The present study highlights the mechanism of the effect of CTX treatment and of the underlying ischemia-induced neuronal damage.