Oxidative Damage of the Extracts of Condensate, Particulate and Semivolatile Organic Compounds from Gasoline Engine Exhausts on Testicles of Rats

Che, Wangjun; Qiu, Hong; Liu, Guiming; Ran, Yun; Zhang, Hao; Zhang, Li; Wen, Weihua

doi:10.1007/s00128-009-9757-x

Cited by 8 publications

(10 citation statements)

References 13 publications

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“…Ovary and testis, both of which show high ALDH3B1 protein and mRNA expression, are also sensitive to oxidative stress processes. In the testis, oxidative stress and the production of 4HNE impair spermatogenesis [5] and environmental pollutants cause increased aldehydes, aldehyde-protein adducts and DNA damage [71]. Expression of ALDH3B1 in the eye is also interesting as the sequence-related ALDH3A1 plays a critical role in protecting ocular structures from oxidative damage [22].…”

Section: Discussionmentioning

confidence: 99%

Molecular characterization, expression analysis, and role of ALDH3B1 in the cellular protection against oxidative stress

Marchitti¹,

Brocker²,

Orlicky³

et al. 2010

Free Radical Biology and Medicine

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Aldehyde dehydrogenase (ALDH) enzymes are critical in the detoxification of aldehydes. The human genome contains 19 ALDH genes, mutations in which are the basis of several diseases. The expression, subcellular localization, enzyme kinetics and role of ALDH3B1 against aldehyde- and oxidant-induced cytotoxicity were investigated. ALDH3B1 was purified from Sf9 cells using chromatographic methods and enzyme kinetics were determined spectrophotometrically. ALDH3B1 demonstrated high affinity for hexanal (Km 62 μM), octanal (Km 8 μM), 4-hydroxy-2-nonenal (4HNE) (Km 52 μM) and benzaldehyde (Km 46 μM). Low affinity was seen towards acetaldehyde (Km 23.3 mM), malondialdehyde (Km 152 mM) and the ester p-nitrophenylacetate (Km 3.6 mM). ALDH3B1 mRNA was abundant in testis, lung, kidney and ovary. ALDH3B1 protein was highly expressed in these tissues and the liver. Immunofluorescence microscopy of ALDH3B1-transfected human embryonic kidney (HEK293) cells and subcellular fractionation of mouse kidney and liver revealed a cytosolic protein localization. ALDH3B1-transfected HEK293 cells were significantly protected from the lipid peroxidation-derived aldehydes trans-2-octenal, 4HNE and hexanal, and the oxidants H2O2 and menadione. In addition, ALDH3B1 protein expression was up-regulated by 4HNE in ARPE-19 cells. The results detailed in this study support a pathophysiological role for ALDH3B1 in protecting cells from the damaging effects of oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Molecular characterization, expression analysis, and role of ALDH3B1 in the cellular protection against oxidative stress

Marchitti¹,

Brocker²,

Orlicky³

et al. 2010

Free Radical Biology and Medicine

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“…After exposure, the levels of malondialdehyde (MDA) and carbonyl protein (CP) were significantly increased, and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) were decreased in the testis. Additionally, DNA single strand breaks were more prominent in the testis by comet assay …”

Section: Effects Of Postnatal Exposure Of Motor Vehicle Exhaust On Ma...mentioning

confidence: 99%

Effects of Motor Vehicle Exhaust on Male Reproductive Function and Associated Proteins

2014

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Air pollution is consistently associated with various diseases and subsequent death among children, adult, and elderly people worldwide. Motor vehicle exhaust contributes to a large proportion of the air pollution present. The motor vehicle exhaust systems emit a variety of toxic components, including carbon monoxide, nitrogen oxides, volatile organic compounds, ozone, particulate matter, and polycyclic aromatic hydrocarbons. Several epidemiological studies and laboratory studies have demonstrated that these components are potentially mutagenic, carcinogenic, and endocrine disrupting agents. However, their impact on male reproductive function and associated proteins is not very clear. Therefore, a comprehensive review on the effects of motor vehicle exhaust on male reproductive function and associated proteins is needed to better understand the risks of exhaust exposure for men. We found that motor vehicle exhaust can cause harmful effects on male reproductive functions by altering organ weights, reducing the spermatozoa qualities, and inducing oxidative stress. Remarkably, motor vehicle exhaust exposure causes significant changes in the expression patterns of proteins that are key components involved in spermatogenesis and testosterone synthesis. In conclusion, this review helps to describe the risks of vehicle exhaust exposure and its relationship to potential adverse effects on the male reproduction system.

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“…Lipid peroxidation, which is a normal phenomenon that occurs continuously at low levels in every individual, is the most common consequence of oxidative stress (Abbassi et al, 2010; Ozyurt et al, 2007). Increased oxygen radical generation and enhanced lipid peroxidation are associated with the pathogenesis of many diseases such as acute myocardial infarction (Ohlin et al, 1998), cholestasis (Copple et al, 2010), breast cancer (Gago-Dominguez et al, 2005), and the toxic activities of various compounds (Che et al, 2009; Duzguner and Kaya, 2007; Dabas et al, 2012; K Chandra et al, 2012). SOD, T-AOC, and GSH are widely accepted as the most important physiological antioxidants against free radicals and can prevent subsequent lipid peroxidation.…”

Section: Discussionmentioning

confidence: 99%

Reproductive toxicity in male mice after exposure to high molybdenum and low copper concentrations

Wang

Zhang²,

Guo³

et al. 2016

Toxicol Ind Health

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To evaluate the effects of dietary high molybdenum (HMo) and low copper (LCu) concentrations on reproductive toxicity of male mice, 80 mice were divided into 4 groups of 20. These groups were fed with the following: (1) normal control (NC) diet (NC group); (2) NC and HMo diets (HMo group); (3) LCu diet (LCu group); and (4) HMo and LCu diets (HMoLCu group). On the 50th and 100th day, superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px), and total antioxidant capacity (T-AOC) were analyzed to determine oxidative stress states. Morphological changes in testicular tissue were evaluated with hematoxylin and eosin staining and ultrastructural changes were monitored by transmission electron microscopy. The results showed that administration of HMo, LCu, and HMoLCu not only decreased sperm density and motility but also increased the rate of teratosperm occurrence. A significant increase in MDA content and a decrease in SOD, GSH-Px, and T-AOC contents were observed in LCu, HMo, and HMoLCu groups. Testicular tissues and cells of mice were damaged by HMo and the damages were more serious in the case of Cu deficiency. Exposure to HMo adversely affected the reproductive system of male mice, and dietary LCu plays key roles in HMo-induced reproductive toxicity.

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Oxidative Damage of the Extracts of Condensate, Particulate and Semivolatile Organic Compounds from Gasoline Engine Exhausts on Testicles of Rats

Cited by 8 publications

References 13 publications

Molecular characterization, expression analysis, and role of ALDH3B1 in the cellular protection against oxidative stress

Molecular characterization, expression analysis, and role of ALDH3B1 in the cellular protection against oxidative stress

Effects of Motor Vehicle Exhaust on Male Reproductive Function and Associated Proteins

Reproductive toxicity in male mice after exposure to high molybdenum and low copper concentrations

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